M. Ghosh, Bhaskar Basu, Gouranga Saha, Shreyasee Ghatak Choudhury
The ubiquitin specific protease USP7/HAUSP is a major deubiquitinase that acts upon a wide spectrum of substrate proteins. Deubiquitination by USP7 generally leads to stabilization of substrates and their rescue from proteasomal degradation, but can also lead to alteration in their intracellular localization and activity. On the basis of its substrate proteins, USP7 has been shown to regulate processes involved in both the maintenance of homeostasis and the promotion of tumorigenesis. USP7, so far does not seem to be a dedicated regulator for either of these cellular phenomena, instead the relative abundance of a particular set of substrates over another being the factor that decides towards which phenomena it will be monopolized. The onset of cancer unfortunately creates an abundance of pro-oncogenic substrates, and this leads to a drastic monopolization of USP7 function towards the enhancement of further pro-oncogenic signaling.
{"title":"Cellular Homeostasis or Tumorigenesis: USP7 Playing the Double Agent","authors":"M. Ghosh, Bhaskar Basu, Gouranga Saha, Shreyasee Ghatak Choudhury","doi":"10.14800/CCM.1624","DOIUrl":"https://doi.org/10.14800/CCM.1624","url":null,"abstract":"The ubiquitin specific protease USP7/HAUSP is a major deubiquitinase that acts upon a wide spectrum of substrate proteins. Deubiquitination by USP7 generally leads to stabilization of substrates and their rescue from proteasomal degradation, but can also lead to alteration in their intracellular localization and activity. On the basis of its substrate proteins, USP7 has been shown to regulate processes involved in both the maintenance of homeostasis and the promotion of tumorigenesis. USP7, so far does not seem to be a dedicated regulator for either of these cellular phenomena, instead the relative abundance of a particular set of substrates over another being the factor that decides towards which phenomena it will be monopolized. The onset of cancer unfortunately creates an abundance of pro-oncogenic substrates, and this leads to a drastic monopolization of USP7 function towards the enhancement of further pro-oncogenic signaling.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"18 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89132577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Bhattacharjee, Pritam Biswas, Sukhamoy Dhabal, Payel Das, Pradip Das, S. Swaroop, Tuhina Prasad, J. Dhanalakshmi, S. Indhumathi
Monoamine oxidase A (MAO-A) is a flavoenzyme that catalyzes biogenic amines into the corresponding aldehydes by oxidative deamination. Although MAO-A is primarily associated with depression and antisocial behaviour, dysregulation of MAO-A has been associated with neurodegenerative diseases and cardiovascular disorders. Moreover, the contribution of MAO-A in the resolution of inflammation is well established. Recent reports reveal the unanticipated role of MAO-A in tumorigenesis. In this review we provide informations that MAO-A is involved in the progression and metastasis of many different cancer cells including prostate cancer, colorectal cancer, hepatocellular carcinoma and lung cancer. We further discuss the regulatory mechanisms that control tumorigenesis, progression and metastasis in these different type of cancer cells. Altogether these informations indicate that MAO-A can be a general therapeutic target in cancer treatment.
我们进一步讨论了在这些不同类型的癌细胞中控制肿瘤发生、进展和转移的调控机制。
{"title":"Role of Monoamine oxidase A (MAO-A) in cancer progression and metastasis","authors":"A. Bhattacharjee, Pritam Biswas, Sukhamoy Dhabal, Payel Das, Pradip Das, S. Swaroop, Tuhina Prasad, J. Dhanalakshmi, S. Indhumathi","doi":"10.14800/CCM.1623","DOIUrl":"https://doi.org/10.14800/CCM.1623","url":null,"abstract":"Monoamine oxidase A (MAO-A) is a flavoenzyme that catalyzes biogenic amines into the corresponding aldehydes by oxidative deamination. Although MAO-A is primarily associated with depression and antisocial behaviour, dysregulation of MAO-A has been associated with neurodegenerative diseases and cardiovascular disorders. Moreover, the contribution of MAO-A in the resolution of inflammation is well established. Recent reports reveal the unanticipated role of MAO-A in tumorigenesis. In this review we provide informations that MAO-A is involved in the progression and metastasis of many different cancer cells including prostate cancer, colorectal cancer, hepatocellular carcinoma and lung cancer. We further discuss the regulatory mechanisms that control tumorigenesis, progression and metastasis in these different type of cancer cells. Altogether these informations indicate that MAO-A can be a general therapeutic target in cancer treatment.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"7 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76372854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Thymoma is a rare neoplasm of thymic epithetical cells that has the ability to spread by local extension. While metastases are most commonly confined to the pleura, pericardium and diaphragm, cases of abdominal metastases have been reported. In a recent publication [ref 7], we conducted a SEER database and literature review to identify cases of malignant thymoma (MT) and abdominal metastases, demonstrating an increasing overall incidence of MT with a significant male predominance. Additionally, we suggested routine screening for all MT patients as roughly 50% of abdominal metastasis cases presented as asymptomatic, as well as a multimodal treatment approach for those with metastatic MT to the abdomen. In this highlight, we briefly present the evidence for a rising rate of MT, review reported cases of abdominal metastasis, and emphasize the need for a multimodal treatment approach.
{"title":"Research Highlight: Metastatic Malignant Thymoma to the Abdomen","authors":"S. Joseph","doi":"10.14800/CCM.1621","DOIUrl":"https://doi.org/10.14800/CCM.1621","url":null,"abstract":"Thymoma is a rare neoplasm of thymic epithetical cells that has the ability to spread by local extension. While metastases are most commonly confined to the pleura, pericardium and diaphragm, cases of abdominal metastases have been reported. In a recent publication [ref 7], we conducted a SEER database and literature review to identify cases of malignant thymoma (MT) and abdominal metastases, demonstrating an increasing overall incidence of MT with a significant male predominance. Additionally, we suggested routine screening for all MT patients as roughly 50% of abdominal metastasis cases presented as asymptomatic, as well as a multimodal treatment approach for those with metastatic MT to the abdomen. In this highlight, we briefly present the evidence for a rising rate of MT, review reported cases of abdominal metastasis, and emphasize the need for a multimodal treatment approach.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78916742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-01-01Epub Date: 2018-04-09DOI: 10.14800/ccm.1630
Bridgette E Drummond, Rebecca A Wingert
Specialized renal epithelial cells known as podocytes are essential components of the filtering structures within the kidney that coordinate the process of removing waste from the bloodstream. Podocyte loss initiates many human kidney diseases as it triggers subsequent damage to the kidney, leading to progressive loss of function that culminates with end stage renal failure. Podocyte morphology, function and gene expression profiles are well conserved between zebrafish and humans, making the former a relevant model to study podocyte development and model kidney diseases. Recently, we reported that whole genome sequencing of the zeppelin (zep) zebrafish mutant, which exhibits podocyte abrogation, revealed that the causative lesion for this defect was a splicing mutation in the breast cancer 2, early onset (brca2) gene. This was a surprising and novel discovery, as previous research on brca2/BRCA2 in a number of vertebrate animal models had not implicated an explicit role for this gene in kidney mesoderm development. Interestingly, the abrogation of the podocyte lineage in zep mutants was also accompanied by the formation of a larger interrenal (IR) gland, which is analogous to the adrenal gland in mammals, and suggested a fate switch between the renal and inter renal mesodermal derivatives. Mirroring these findings, knockdown of brca2 also recapitulated the loss of podocytes and increased IR population. In addition, brca2 overexpression was sufficient to partially rescue podocytes in zep mutants, and induced ectopic podocyte formation in wild-type embryos. Interestingly, immunofluorescence studies indicated that zep mutants had elevated P-h2A.X levels, suggesting that DNA repair is dysfunctional in these animals and contributes to the zep phenotype. Moving forward, this unique zebrafish mutant provides a new model to further explore how brca2 contributes to the development of tissues including the kidney mesoderm-roles which may have implications for renal diseases as well.
{"title":"Scaling up to study <i>brca2</i>: the <i>zeppelin</i> zebrafish mutant reveals a role for <i>brca2</i> in embryonic development of kidney mesoderm.","authors":"Bridgette E Drummond, Rebecca A Wingert","doi":"10.14800/ccm.1630","DOIUrl":"https://doi.org/10.14800/ccm.1630","url":null,"abstract":"<p><p>Specialized renal epithelial cells known as podocytes are essential components of the filtering structures within the kidney that coordinate the process of removing waste from the bloodstream. Podocyte loss initiates many human kidney diseases as it triggers subsequent damage to the kidney, leading to progressive loss of function that culminates with end stage renal failure. Podocyte morphology, function and gene expression profiles are well conserved between zebrafish and humans, making the former a relevant model to study podocyte development and model kidney diseases. Recently, we reported that whole genome sequencing of the <i>zeppelin (zep)</i> zebrafish mutant, which exhibits podocyte abrogation, revealed that the causative lesion for this defect was a splicing mutation in the <i>breast cancer 2, early onset</i> (<i>brca2</i>) gene. This was a surprising and novel discovery, as previous research on <i>brca2/BRCA2</i> in a number of vertebrate animal models had not implicated an explicit role for this gene in kidney mesoderm development. Interestingly, the abrogation of the podocyte lineage in <i>zep</i> mutants was also accompanied by the formation of a larger interrenal (IR) gland, which is analogous to the adrenal gland in mammals, and suggested a fate switch between the renal and inter renal mesodermal derivatives. Mirroring these findings, knockdown of <i>brca2</i> also recapitulated the loss of podocytes and increased IR population. In addition, <i>brca2</i> overexpression was sufficient to partially rescue podocytes in <i>zep</i> mutants, and induced ectopic podocyte formation in wild-type embryos. Interestingly, immunofluorescence studies indicated that <i>zep</i> mutants had elevated P-h2A.X levels, suggesting that DNA repair is dysfunctional in these animals and contributes to the <i>zep</i> phenotype. Moving forward, this unique zebrafish mutant provides a new model to further explore how <i>brca2</i> contributes to the development of tissues including the kidney mesoderm-roles which may have implications for renal diseases as well.</p>","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5922780/pdf/nihms960319.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36054026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cryptotanshinone (CPT) is a lipid-soluble constituent isolated from the root of Salvia Miltiorrhiza Bunge. Except the widely known antimicrobial, cardioprotection and antiinflammation effect, recent studies emphasize the potent anticancer activity of CPT in a wide variety of human cancers. Our previous study paid attention to the function of CPT against RCC. Results demonstrated that CPT could significantly suppress RCC formation in vitro and in vivo as a specific STAT3 inhibitor, indicating the potential therapeutic value of CPT against RCC.
{"title":"Cryptotanshinone suppresses cell proliferation and induces apoptosis in renal cell carcinoma as an STAT3 inhibitor","authors":"W. Zhai","doi":"10.14800/ccm.1607","DOIUrl":"https://doi.org/10.14800/ccm.1607","url":null,"abstract":"Cryptotanshinone (CPT) is a lipid-soluble constituent isolated from the root of Salvia Miltiorrhiza Bunge. Except the widely known antimicrobial, cardioprotection and antiinflammation effect, recent studies emphasize the potent anticancer activity of CPT in a wide variety of human cancers. Our previous study paid attention to the function of CPT against RCC. Results demonstrated that CPT could significantly suppress RCC formation in vitro and in vivo as a specific STAT3 inhibitor, indicating the potential therapeutic value of CPT against RCC.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"254 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79486478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Huining Bai, Lily Li, Zhen Ji, Cong Wang, Weijia Wen
The photoinduced effects of nanomaterials encompass several incredibly hot research topics, including the photoelectric, photothermal (PT) and photochemical effects. The PT effect arises from the synergistic effect between light irradiation and heat diffusion and has potential uses in cancer therapy and antimicrobial materials. Meanwhile, the photo-Fenton (PF) reaction is a typical photochemical reaction that has become an important method for combating environmental waste and organisms. Here, the development of the PT effect and PF reaction of nanoparticles (NPs) has been reviewed. Considerable attention has been paid to the tremendous wide range of nanomaterial types, such as oxide/sulfide, carbon-based NPs and metallic NPs, that can provide a photoheat or photochemical response and for determining the optimal dose for each material. The main focus of this review is the development and physicochemical mechanisms of each classical compound type as well as the application of photoresponsive nanomaterials in therapy and disinfection.
{"title":"Photoinduced antitumor and antimicrobial effects of nanomaterials","authors":"Huining Bai, Lily Li, Zhen Ji, Cong Wang, Weijia Wen","doi":"10.14800/CCM.1606","DOIUrl":"https://doi.org/10.14800/CCM.1606","url":null,"abstract":"The photoinduced effects of nanomaterials encompass several incredibly hot research topics, including the photoelectric, photothermal (PT) and photochemical effects. The PT effect arises from the synergistic effect between light irradiation and heat diffusion and has potential uses in cancer therapy and antimicrobial materials. Meanwhile, the photo-Fenton (PF) reaction is a typical photochemical reaction that has become an important method for combating environmental waste and organisms. Here, the development of the PT effect and PF reaction of nanoparticles (NPs) has been reviewed. Considerable attention has been paid to the tremendous wide range of nanomaterial types, such as oxide/sulfide, carbon-based NPs and metallic NPs, that can provide a photoheat or photochemical response and for determining the optimal dose for each material. The main focus of this review is the development and physicochemical mechanisms of each classical compound type as well as the application of photoresponsive nanomaterials in therapy and disinfection.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"98 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81178868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Treatment of cancer is frequently unsuccessful related to the loss of apoptotic signaling in malignant cells. This is a particular problem for high-grade gliomas, such as Glioblastoma Multiforme (GBM), which are almost universally fatal within a year or so of diagnosis. Novel therapies that capitalize on non-apoptotic cell death pathways may yield more effective outcomes, if their underlying mechanisms can be more completely deciphered. In a recent publication (ref 10), the mechanisms by which cellular cyclophilins support GBM cell survival have been identified. Inhibition of cyclophilins activated paraptosis, which relied on a combination of endoplasmic reticulum (ER) stress and transient activation of autophagy. An important aspect of this effect was the relative rates of cap-dependent versus cap-independent protein synthesis, which were differentially modulated by protein synthesis inhibitors or mTOR inhibition. Although cycloheximide has previously been characterized as an inhibitor of paraptosis, in the case of cyclophilin inhibition, it appears to significantly enhance stress-related paraptosis and cell death. This work reveals an important role for cap-independent protein translation and autophagy in the ability of GBM cells to resist non-apoptotic death, and adds to our understanding of the events that underlie paraptosis.
{"title":"Protein synthesis inhibition enhances paraptotic death induced by inhibition of cyclophilins in glioblastoma cells","authors":"Lin Wang, Justin H. Gundelach, R. Bram","doi":"10.14800/CCM.1601","DOIUrl":"https://doi.org/10.14800/CCM.1601","url":null,"abstract":"Treatment of cancer is frequently unsuccessful related to the loss of apoptotic signaling in malignant cells. This is a particular problem for high-grade gliomas, such as Glioblastoma Multiforme (GBM), which are almost universally fatal within a year or so of diagnosis. Novel therapies that capitalize on non-apoptotic cell death pathways may yield more effective outcomes, if their underlying mechanisms can be more completely deciphered. In a recent publication (ref 10), the mechanisms by which cellular cyclophilins support GBM cell survival have been identified. Inhibition of cyclophilins activated paraptosis, which relied on a combination of endoplasmic reticulum (ER) stress and transient activation of autophagy. An important aspect of this effect was the relative rates of cap-dependent versus cap-independent protein synthesis, which were differentially modulated by protein synthesis inhibitors or mTOR inhibition. Although cycloheximide has previously been characterized as an inhibitor of paraptosis, in the case of cyclophilin inhibition, it appears to significantly enhance stress-related paraptosis and cell death. This work reveals an important role for cap-independent protein translation and autophagy in the ability of GBM cells to resist non-apoptotic death, and adds to our understanding of the events that underlie paraptosis.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"39 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74463360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hongyan Liu, Lianlian Li, Xiaoyu Zhang, Dayong Cui
Alternative splicing contributes to the vast complexity of mRNA transcripts and protein isoforms. It has been estimated that the majority of protein-coding genes are subject to alternative splicing in humans. Alternative splicing plays a critical role in physiological processes and cell development programs, and dysregulation of alternative splicing is often associated with pathologic conditions such as cancer. Indeed, the abnormal splicing is frequently found in lung cancer, which produces various protein isoforms with properties that may have different functions and therefore even diverse effects on tumor malignant development. In this highlight, we summarize the evidence supporting the functional role of alternative splicing in lung cancer, discuss the regulation of alternative splicing, and highlight the relevance of splicing variation on lung cancer therapy.
{"title":"Roles of alternative splicing in the pathogenesis of lung cancer","authors":"Hongyan Liu, Lianlian Li, Xiaoyu Zhang, Dayong Cui","doi":"10.14800/CCM.1596","DOIUrl":"https://doi.org/10.14800/CCM.1596","url":null,"abstract":"Alternative splicing contributes to the vast complexity of mRNA transcripts and protein isoforms. It has been estimated that the majority of protein-coding genes are subject to alternative splicing in humans. Alternative splicing plays a critical role in physiological processes and cell development programs, and dysregulation of alternative splicing is often associated with pathologic conditions such as cancer. Indeed, the abnormal splicing is frequently found in lung cancer, which produces various protein isoforms with properties that may have different functions and therefore even diverse effects on tumor malignant development. In this highlight, we summarize the evidence supporting the functional role of alternative splicing in lung cancer, discuss the regulation of alternative splicing, and highlight the relevance of splicing variation on lung cancer therapy.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"102 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80506170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cancer stem cells (CSC) are a group of cells with capacity of self renewal and can proliferate into a heterogeneous bulk with cancer progeny population. This is the exactly primary reason for metastasis and recurrence of tumors. Strategies for studying cancer’s targeted therapy and biological property mainly include its isolation and enrichment. In the coming era it will also be the focus of significant value. We will summarize the current strategies used for isolation and enrichment of CSC, including serum-free suspension culture, feeder cell layers, immunoselection based on cell surface markers, side population cells, resistance to radiation treatment and chemotherapy, combined utilization of various strategies and a three dimension (3D) in vitro model in this review.
{"title":"Progress in Isolation and Enrichment of Cancer Stem Cells","authors":"Chanchan Zhu, Qing Sun","doi":"10.14800/CCM.1575","DOIUrl":"https://doi.org/10.14800/CCM.1575","url":null,"abstract":"Cancer stem cells (CSC) are a group of cells with capacity of self renewal and can proliferate into a heterogeneous bulk with cancer progeny population. This is the exactly primary reason for metastasis and recurrence of tumors. Strategies for studying cancer’s targeted therapy and biological property mainly include its isolation and enrichment. In the coming era it will also be the focus of significant value. We will summarize the current strategies used for isolation and enrichment of CSC, including serum-free suspension culture, feeder cell layers, immunoselection based on cell surface markers, side population cells, resistance to radiation treatment and chemotherapy, combined utilization of various strategies and a three dimension (3D) in vitro model in this review.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"7 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91502738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Trichosanthin (TCS), known as a plant toxin, is applied as a midterm abortifacient in clinics, and currently reported to exhibit other biological and pharmaceutical effects such as anti-tumor, anti-HIV, and Immunoregulation. TCS was found out to firmly inactivate the ribosomes of the eukaryotic cell, but this finding was far enough to explain its various biological and pharmaceutical effects. Our previous studies focused on exploring novel TCS binding proteins, as to reveal new mechanisms in mammalian cells. And we found out that TCS and cation-independent mannose-6-phosphate receptor (CI-MPR) competitively bind to Golgi-localized, γ-ear containing and Arf-binding proteins (GGA), which finally increased the cell permeability of Granzyme B and promoted the cytotoxic T lymphocyte-mediated tumor cell apoptosis.
{"title":"Trichosanthin induces anti-cancer effects by increasing the penetration of Granzyme B into tumor cells","authors":"Yinxin Zhu, D. Ye, Jing Shen, Zhangang Xiao","doi":"10.14800/ccm.1576","DOIUrl":"https://doi.org/10.14800/ccm.1576","url":null,"abstract":"Trichosanthin (TCS), known as a plant toxin, is applied as a midterm abortifacient in clinics, and currently reported to exhibit other biological and pharmaceutical effects such as anti-tumor, anti-HIV, and Immunoregulation. TCS was found out to firmly inactivate the ribosomes of the eukaryotic cell, but this finding was far enough to explain its various biological and pharmaceutical effects. Our previous studies focused on exploring novel TCS binding proteins, as to reveal new mechanisms in mammalian cells. And we found out that TCS and cation-independent mannose-6-phosphate receptor (CI-MPR) competitively bind to Golgi-localized, γ-ear containing and Arf-binding proteins (GGA), which finally increased the cell permeability of Granzyme B and promoted the cytotoxic T lymphocyte-mediated tumor cell apoptosis.","PeriodicalId":9576,"journal":{"name":"Cancer cell & microenvironment","volume":"14 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76448597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：