Exosomes are nanovesicles derived from multiple cell types and could be isolated from various bodily fluids, such as blood and saliva. The molecular contents of exosomes have been proved to reflect their parent cell origins. MicroRNA (miRNA), a large family of small, noncoding RNAs, is enriched in exosomes and could regulate the expression of their target genes. Numerous studies have indicated that aberrant expression level of exosomal miRNAs is closely related to the onset of multiple diseases, including cancer. For example, the studies show that tumorigenesis, drug resistance, invasiveness, and metastasis in breast cancer, are partly mediated by exosome miRNAs, functioning as tools for cell-to-cell communication. Furthermore, several investigations have revealed the immense potential of exosome miRNAs to serve as prognostic and diagnostic biomarkers, whereas certain miRNAs could even be on the target list of novel therapies for cancer, including breast cancer. Due to the lack of a standard approach, exosome miRNAs have not been successfully made into clinical practice, yet. In this review, we highlight the major progressions in exosome miRNA research on breast cancer and the current limitations/challenges in its clinical implementation. Promising and potential applications of exosomal miRNAs will also be addressed.
{"title":"Role of exosome microRNA in breast cancer","authors":"W. Qu, Ma Fei, Bing-he Xu","doi":"10.4103/ctm.ctm_14_17","DOIUrl":"https://doi.org/10.4103/ctm.ctm_14_17","url":null,"abstract":"Exosomes are nanovesicles derived from multiple cell types and could be isolated from various bodily fluids, such as blood and saliva. The molecular contents of exosomes have been proved to reflect their parent cell origins. MicroRNA (miRNA), a large family of small, noncoding RNAs, is enriched in exosomes and could regulate the expression of their target genes. Numerous studies have indicated that aberrant expression level of exosomal miRNAs is closely related to the onset of multiple diseases, including cancer. For example, the studies show that tumorigenesis, drug resistance, invasiveness, and metastasis in breast cancer, are partly mediated by exosome miRNAs, functioning as tools for cell-to-cell communication. Furthermore, several investigations have revealed the immense potential of exosome miRNAs to serve as prognostic and diagnostic biomarkers, whereas certain miRNAs could even be on the target list of novel therapies for cancer, including breast cancer. Due to the lack of a standard approach, exosome miRNAs have not been successfully made into clinical practice, yet. In this review, we highlight the major progressions in exosome miRNA research on breast cancer and the current limitations/challenges in its clinical implementation. Promising and potential applications of exosomal miRNAs will also be addressed.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"152 1","pages":"167 - 173"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86786987","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 : 2016-11-01DOI: 10.4103/2395-3977.196910
J. Lacal, L. Andĕra
Aim: The aim of this study was to investigate the effects of the combination of choline kinase inhibitor MN58b and tumor necrosis factor-related apoptosis inducing ligand (TRAIL) against colon cancer cells. Methods: TRAIL-sensitive (DLD-1) and TRAIL-resistant (SW620) cells were treated with MN58b and/or TRAIL. Cell viability and induction of apoptosis were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide and flow cytometry. Posttreatment expression levels of different proteins (PARP, caspase-3, X-linked inhibitor of apoptosis protein [XIAP], CHOP, DR5, DR4, CHOP) were analyzed by quantitative reverse transcription polymerase chain reaction, Western blot, and flow cytometry.In vivo antitumoral activity was assessed by xenograft models. Results: A strong synergistic effect of TRAIL and MN58b was observed in both TRAIL-sensitive and resistant cells. The combinatory treatment induced an increase in PARP and active-caspase 3 fragments along with a decrease in XIAP, enhancing TRAIL sensitivity. Reduced cellular viability and increased cell death correlated with increased DR5 expression and membrane surface recruitment, an effect that was concomitant with CHOP expression. Conclusion: MN58b, which alone exhibits anticancer activities against a wide variety of tumor-derived cell lines, synergizes with TRAIL through a mechanism that involves DR5 upregulation. This study supports the use of MN58b in combination with TRAIL on colorectal tumors, including those that develop TRAIL resistance.
目的:探讨胆碱激酶抑制剂MN58b联合肿瘤坏死因子相关凋亡诱导配体(TRAIL)对结肠癌细胞的作用。方法:用MN58b和/或TRAIL处理TRAIL敏感细胞(DLD-1)和TRAIL耐药细胞(SW620)。采用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四唑和流式细胞术检测细胞活力和诱导凋亡情况。通过定量逆转录聚合酶链反应、Western blot和流式细胞术分析处理后不同蛋白(PARP、caspase-3、X-linked inhibitor of apoptosis protein [XIAP]、CHOP、DR5、DR4、CHOP)的表达水平。通过异种移植物模型评估体内抗肿瘤活性。结果:TRAIL和MN58b在TRAIL敏感和耐药细胞中均有较强的协同作用。联合治疗导致PARP和活性caspase 3片段增加，XIAP减少，TRAIL敏感性增强。细胞活力的降低和细胞死亡的增加与DR5表达和膜表面募集的增加有关，这种效应伴随着CHOP的表达。结论:MN58b单独对多种肿瘤源性细胞系表现出抗癌活性，其与TRAIL的协同作用机制涉及DR5上调。本研究支持MN58b联合TRAIL治疗结直肠肿瘤，包括那些产生TRAIL耐药性的结直肠肿瘤。
{"title":"Choline kinase inhibitors synergize with TRAIL in the treatment of colorectal tumors and overcomes TRAIL resistance","authors":"J. Lacal, L. Andĕra","doi":"10.4103/2395-3977.196910","DOIUrl":"https://doi.org/10.4103/2395-3977.196910","url":null,"abstract":"Aim: The aim of this study was to investigate the effects of the combination of choline kinase inhibitor MN58b and tumor necrosis factor-related apoptosis inducing ligand (TRAIL) against colon cancer cells. Methods: TRAIL-sensitive (DLD-1) and TRAIL-resistant (SW620) cells were treated with MN58b and/or TRAIL. Cell viability and induction of apoptosis were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide and flow cytometry. Posttreatment expression levels of different proteins (PARP, caspase-3, X-linked inhibitor of apoptosis protein [XIAP], CHOP, DR5, DR4, CHOP) were analyzed by quantitative reverse transcription polymerase chain reaction, Western blot, and flow cytometry.In vivo antitumoral activity was assessed by xenograft models. Results: A strong synergistic effect of TRAIL and MN58b was observed in both TRAIL-sensitive and resistant cells. The combinatory treatment induced an increase in PARP and active-caspase 3 fragments along with a decrease in XIAP, enhancing TRAIL sensitivity. Reduced cellular viability and increased cell death correlated with increased DR5 expression and membrane surface recruitment, an effect that was concomitant with CHOP expression. Conclusion: MN58b, which alone exhibits anticancer activities against a wide variety of tumor-derived cell lines, synergizes with TRAIL through a mechanism that involves DR5 upregulation. This study supports the use of MN58b in combination with TRAIL on colorectal tumors, including those that develop TRAIL resistance.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"62 1","pages":"163 - 174"},"PeriodicalIF":0.0,"publicationDate":"2016-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85560876","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 : 2016-11-01DOI: 10.4103/2395-3977.196913
Marco Pérez, L. Navas, A. Carnero
Basic research and clinical trials are essential components of the process of discovery and development of new drugs. The use of preclinical models is a key component in every aspect of drug development in cancer. Unfortunately, preclinical models often fail to capture the diverse heterogeneity of human malignancies, and the correlation between the antitumor activity of cytotoxic agents observed in these animal models and that observed in humans is poor. In recent years, there has been an increasing interest in the application of preclinical cancer models which can actually recapitulate the clinical disease, including patient-derived xenografts (PDXs). PDX models maintain the phenotypic, genetic, and molecular characteristics of the original tumor and reflect tumor pathology. This review discusses the limitation of the conventional strategy of developing new drugs in oncology and proposes the PDX models as a powerful technology for the biological study of tumors and to evaluate the antitumoral effect of new compounds.
{"title":"Patient-derived xenografts as models for personalized medicine research in cancer","authors":"Marco Pérez, L. Navas, A. Carnero","doi":"10.4103/2395-3977.196913","DOIUrl":"https://doi.org/10.4103/2395-3977.196913","url":null,"abstract":"Basic research and clinical trials are essential components of the process of discovery and development of new drugs. The use of preclinical models is a key component in every aspect of drug development in cancer. Unfortunately, preclinical models often fail to capture the diverse heterogeneity of human malignancies, and the correlation between the antitumor activity of cytotoxic agents observed in these animal models and that observed in humans is poor. In recent years, there has been an increasing interest in the application of preclinical cancer models which can actually recapitulate the clinical disease, including patient-derived xenografts (PDXs). PDX models maintain the phenotypic, genetic, and molecular characteristics of the original tumor and reflect tumor pathology. This review discusses the limitation of the conventional strategy of developing new drugs in oncology and proposes the PDX models as a powerful technology for the biological study of tumors and to evaluate the antitumoral effect of new compounds.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"8 1","pages":"197 - 202"},"PeriodicalIF":0.0,"publicationDate":"2016-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89499148","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 : 2016-11-01DOI: 10.4103/2395-3977.196912
M. Jiménez-García, E. Verdugo-Sivianes, Antonio Lucena-Cacace
Gliomas are highly metabolically active tumors. Cancer metabolism is currently of great interest to researchers. Nicotinamide adenine dinucleotide (NAD) is central in cell metabolism. NAD+ plays a crucial role in a wide spectrum of metabolic processes in the cancer metabolism, boosting and feeding enzymes as a cofactor, and is an important driver in metabolic reprograming. NAD+ biology goes through the most essential pathways helping to derive energy in multiple ways, depicting one the most important metabolites to maintain cellular homeostasis. Understanding its implication in glioma's biology is of interest for targeted therapies in all pathways, in which NAD+ largely promotes cancer initiation, progression, dissemination, and eventual cellular reprogramation. Here, the essential points of NAD+ biology, its contribution on cellular reprograming, and its therapeutical approaches on glioma treatment are summarized.
{"title":"Nicotinamide adenine dinucleotide+ metabolism biomarkers in malignant gliomas","authors":"M. Jiménez-García, E. Verdugo-Sivianes, Antonio Lucena-Cacace","doi":"10.4103/2395-3977.196912","DOIUrl":"https://doi.org/10.4103/2395-3977.196912","url":null,"abstract":"Gliomas are highly metabolically active tumors. Cancer metabolism is currently of great interest to researchers. Nicotinamide adenine dinucleotide (NAD) is central in cell metabolism. NAD+ plays a crucial role in a wide spectrum of metabolic processes in the cancer metabolism, boosting and feeding enzymes as a cofactor, and is an important driver in metabolic reprograming. NAD+ biology goes through the most essential pathways helping to derive energy in multiple ways, depicting one the most important metabolites to maintain cellular homeostasis. Understanding its implication in glioma's biology is of interest for targeted therapies in all pathways, in which NAD+ largely promotes cancer initiation, progression, dissemination, and eventual cellular reprogramation. Here, the essential points of NAD+ biology, its contribution on cellular reprograming, and its therapeutical approaches on glioma treatment are summarized.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"17 1","pages":"189 - 196"},"PeriodicalIF":0.0,"publicationDate":"2016-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83667972","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 : 2016-11-01DOI: 10.4103/2395-3977.196909
D. Otero-Albiol, B. Felipe-Abrio
Metabolic reprogramming is a feature of cancer cells that provides fast energy production and the abundance of precursors required to fuel uncontrolled proliferation. The Warburg effect, increase in glucose uptake and preference for glycolysis over oxidative phosphorylation (OXPHOS) as major source of energy even in the presence of oxygen, is the main metabolic adaptation of cancer cells but not the only one. Increased glutaminolysis is also observed in cancer cells, being another source of adenosine triphosphate production and supply of intermediates for macromolecule biosynthesis. The ability to shift from OXPHOS to glycolysis and vice versa, known as metabolic plasticity, allows cancer cells to adapt to continuous changes in the tumor microenvironment. Metabolic reprogramming is linked to the deregulation of pathways controlled by hypoxia-inducible factor 1 alpha, MYC, or p53, and microRNAs (miRNAs) have emerged as key regulators of these signaling pathways. miRNAs target metabolic enzymes, oncogenes, and tumor suppressors involved in metabolic reprogramming, becoming crucial elements in the cross talk of molecular pathways that promotes survival, proliferation, migration, and consequently, tumor progression and metastasis. Moreover, several miRNAs have been found downregulated in different human cancers. Due to this fact and their central role in metabolism regulation, miRNAs may be considered as biomarkers for cancer therapy.
{"title":"MicroRNA regulating metabolic reprogramming in tumor cells: New tumor markers","authors":"D. Otero-Albiol, B. Felipe-Abrio","doi":"10.4103/2395-3977.196909","DOIUrl":"https://doi.org/10.4103/2395-3977.196909","url":null,"abstract":"Metabolic reprogramming is a feature of cancer cells that provides fast energy production and the abundance of precursors required to fuel uncontrolled proliferation. The Warburg effect, increase in glucose uptake and preference for glycolysis over oxidative phosphorylation (OXPHOS) as major source of energy even in the presence of oxygen, is the main metabolic adaptation of cancer cells but not the only one. Increased glutaminolysis is also observed in cancer cells, being another source of adenosine triphosphate production and supply of intermediates for macromolecule biosynthesis. The ability to shift from OXPHOS to glycolysis and vice versa, known as metabolic plasticity, allows cancer cells to adapt to continuous changes in the tumor microenvironment. Metabolic reprogramming is linked to the deregulation of pathways controlled by hypoxia-inducible factor 1 alpha, MYC, or p53, and microRNAs (miRNAs) have emerged as key regulators of these signaling pathways. miRNAs target metabolic enzymes, oncogenes, and tumor suppressors involved in metabolic reprogramming, becoming crucial elements in the cross talk of molecular pathways that promotes survival, proliferation, migration, and consequently, tumor progression and metastasis. Moreover, several miRNAs have been found downregulated in different human cancers. Due to this fact and their central role in metabolism regulation, miRNAs may be considered as biomarkers for cancer therapy.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"87 1","pages":"175 - 181"},"PeriodicalIF":0.0,"publicationDate":"2016-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73850626","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 : 2016-11-01DOI: 10.4103/2395-3977.196911
J. Santos-Pereira, S. Muñoz-Galván
Colorectal cancer (CRC) is one of the most common cancers in the world and one of the main causes of death. Although CRC is among the best-studied cancers and our knowledge about CRC biomarkers and carcinogenesis is extensive, there are only a few approved therapies for its treatment, and personalized therapy is far from being achieved. However, the recent advent of the genome-wide techniques, and in particular next-generation sequencing, has notably contributed to our knowledge about CRC genomes. These techniques have allowed not only the identification of new somatic mutations associated with CRC, but also the emergence of novel aspects of CRC genomes previously unanticipated. In this review, we discuss more recent advances in our understanding of CRC genomes, with an emphasis in the contribution of genomics and the development of personalized therapies.
{"title":"Biomarkers of colorectal cancer: A genome-wide perspective","authors":"J. Santos-Pereira, S. Muñoz-Galván","doi":"10.4103/2395-3977.196911","DOIUrl":"https://doi.org/10.4103/2395-3977.196911","url":null,"abstract":"Colorectal cancer (CRC) is one of the most common cancers in the world and one of the main causes of death. Although CRC is among the best-studied cancers and our knowledge about CRC biomarkers and carcinogenesis is extensive, there are only a few approved therapies for its treatment, and personalized therapy is far from being achieved. However, the recent advent of the genome-wide techniques, and in particular next-generation sequencing, has notably contributed to our knowledge about CRC genomes. These techniques have allowed not only the identification of new somatic mutations associated with CRC, but also the emergence of novel aspects of CRC genomes previously unanticipated. In this review, we discuss more recent advances in our understanding of CRC genomes, with an emphasis in the contribution of genomics and the development of personalized therapies.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"21 1","pages":"182 - 188"},"PeriodicalIF":0.0,"publicationDate":"2016-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85520890","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 : 2016-09-01DOI: 10.4103/2395-3977.192931
B. Venkatraman
Triple-negative breast cancer (TNBC) remains a significant clinical and scientific challenge. The classification of TNBC is based on the lack of expression of the human epidermal growth factor 2, the estrogen receptor, and the progesterone receptor. TNBC accounts for more than 20% of all breast cancers (BCs), has a poorer prognosis compared to other BC subtypes, and has no targeted therapeutics. Primarily, this review focuses on the heterogeneity of BC and the importance of molecular subtyping for the accurate classification of TNBC. Further, it seeks to identify the molecular "omic" gaps in subtyping TNBC and the role of membrane protein biomarkers that could potentially advance clinical and translational research in BC.
{"title":"Identifying gaps and relative opportunities for discovering membrane proteomic biomarkers of triple-negative breast cancer as a translational priority","authors":"B. Venkatraman","doi":"10.4103/2395-3977.192931","DOIUrl":"https://doi.org/10.4103/2395-3977.192931","url":null,"abstract":"Triple-negative breast cancer (TNBC) remains a significant clinical and scientific challenge. The classification of TNBC is based on the lack of expression of the human epidermal growth factor 2, the estrogen receptor, and the progesterone receptor. TNBC accounts for more than 20% of all breast cancers (BCs), has a poorer prognosis compared to other BC subtypes, and has no targeted therapeutics. Primarily, this review focuses on the heterogeneity of BC and the importance of molecular subtyping for the accurate classification of TNBC. Further, it seeks to identify the molecular \"omic\" gaps in subtyping TNBC and the role of membrane protein biomarkers that could potentially advance clinical and translational research in BC.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"90 1","pages":"137 - 146"},"PeriodicalIF":0.0,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82367595","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 : 2016-09-01DOI: 10.4103/2395-3977.192932
Zhen Wang, Hongwei Yang, Xin Wang, Liang Wang, Yingduan Cheng, Yongsheng Zhang, Y. Tu
Malignant cancer is among the top of the life-threatening conditions, challenging humanity for a long time. Traditional methods of cancer therapy include surgery, chemotherapy, and radiotherapy, which aim to remove/destroy cancer cells. Although theoretically very promising, none of these methods can effectively eradicate cancer, the reason for which can be attributed to our incomplete understanding of the mechanism of cancer metastasis and recurrence. In recent years, researchers have proposed the theory of cancer stem cell (CSC). CSC is a small population of tumor cells that have unlimited self-renewal ability, exhibit a strong resistance to chemotherapy and radiotherapy, and have been proved to be the core reason of cancer metastasis and recurrence. CSC theory provides a deep insight into malignant tumorigenesis that brings new hope for tumor therapy. In this paper, we intend to discuss the development of CSC theory and summarize the regulatory pathways involved in CSC origin and self-renewal, which might be of assistance in the future development of malignant cancer therapy.
{"title":"The molecular mechanism and regulatory pathways of cancer stem cells","authors":"Zhen Wang, Hongwei Yang, Xin Wang, Liang Wang, Yingduan Cheng, Yongsheng Zhang, Y. Tu","doi":"10.4103/2395-3977.192932","DOIUrl":"https://doi.org/10.4103/2395-3977.192932","url":null,"abstract":"Malignant cancer is among the top of the life-threatening conditions, challenging humanity for a long time. Traditional methods of cancer therapy include surgery, chemotherapy, and radiotherapy, which aim to remove/destroy cancer cells. Although theoretically very promising, none of these methods can effectively eradicate cancer, the reason for which can be attributed to our incomplete understanding of the mechanism of cancer metastasis and recurrence. In recent years, researchers have proposed the theory of cancer stem cell (CSC). CSC is a small population of tumor cells that have unlimited self-renewal ability, exhibit a strong resistance to chemotherapy and radiotherapy, and have been proved to be the core reason of cancer metastasis and recurrence. CSC theory provides a deep insight into malignant tumorigenesis that brings new hope for tumor therapy. In this paper, we intend to discuss the development of CSC theory and summarize the regulatory pathways involved in CSC origin and self-renewal, which might be of assistance in the future development of malignant cancer therapy.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"16 1","pages":"147 - 153"},"PeriodicalIF":0.0,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84605286","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 : 2016-09-01DOI: 10.4103/2395-3977.192933
Wenjin Shi, Ding Weng, Wanting Niu
Being a great threat to human health, with no permanent cure yet, better treatment and further research in cancer are inevitable. Nanoparticle drug delivery systems (NDDSs), especially pH-sensitive NDDSs, such as lipid-based, polymeric, and mesoporous silica nanoparticles have played a significant role in cancer treatments. Further, three-dimensional (3D) cell cultures models, which include tumor spheroid models, microfluidic systems, and matrix/scaffolds-based 3D tumor, better mimic the tumor microenvironment than the conventional two-dimensional cultures, making it possible to better understand the disease while serving as a useful in vitro model for future research. The present review mainly focuses on such 3D cell cultures and drug delivery systems that are applied in cancer research and treatments.
{"title":"Nanoparticle drug delivery systems and three-dimensional cell cultures in cancer treatments and research","authors":"Wenjin Shi, Ding Weng, Wanting Niu","doi":"10.4103/2395-3977.192933","DOIUrl":"https://doi.org/10.4103/2395-3977.192933","url":null,"abstract":"Being a great threat to human health, with no permanent cure yet, better treatment and further research in cancer are inevitable. Nanoparticle drug delivery systems (NDDSs), especially pH-sensitive NDDSs, such as lipid-based, polymeric, and mesoporous silica nanoparticles have played a significant role in cancer treatments. Further, three-dimensional (3D) cell cultures models, which include tumor spheroid models, microfluidic systems, and matrix/scaffolds-based 3D tumor, better mimic the tumor microenvironment than the conventional two-dimensional cultures, making it possible to better understand the disease while serving as a useful in vitro model for future research. The present review mainly focuses on such 3D cell cultures and drug delivery systems that are applied in cancer research and treatments.","PeriodicalId":9428,"journal":{"name":"Cancer Translational Medicine","volume":"82 1","pages":"154 - 161"},"PeriodicalIF":0.0,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83966326","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}
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