Pub Date : 2023-05-18DOI: 10.2174/1573394719666230518112114
M. Alivand, Mahsa Fakeri, Seyed Masoud Armandzadeh, Shabnam Koulaeizadeh, Elmira Aboutalebi Vand Beilankouhi, Mohammad Valilo
microRNAs (miRNA) play a significant role in regulating gene expression at the post-transcriptional level in multicellular organisms, such as mammals. These small non-coding RNAs (snRNA) can be present in plants and even viruses, and make up about 60% of human genes. Many different functions and roles are played by miRNAs, including their role in many diseases and cancers. The results of various studies in recent years on the role of miRNA-337 in cancers have shown that miR-337 acts as a cancer inhibitor and can play a key role in the treatment of various cancers by inhibiting cell invasion. Thus, among the various miRNAs, in this review, we aim to shed light on the function of miR-337 in different types of cancer.
{"title":"Involvement of MiRNA-337 in Various Cancers","authors":"M. Alivand, Mahsa Fakeri, Seyed Masoud Armandzadeh, Shabnam Koulaeizadeh, Elmira Aboutalebi Vand Beilankouhi, Mohammad Valilo","doi":"10.2174/1573394719666230518112114","DOIUrl":"https://doi.org/10.2174/1573394719666230518112114","url":null,"abstract":"\u0000\u0000microRNAs (miRNA) play a significant role in regulating gene expression at the post-transcriptional level in multicellular organisms, such as mammals. These small non-coding RNAs (snRNA) can be present in plants and even viruses, and make up about 60% of human genes. Many different functions and roles are played by miRNAs, including their role in many diseases and cancers. The results of various studies in recent years on the role of miRNA-337 in cancers have shown that miR-337 acts as a cancer inhibitor and can play a key role in the treatment of various cancers by inhibiting cell invasion. Thus, among the various miRNAs, in this review, we aim to shed light on the function of miR-337 in different types of cancer.\u0000","PeriodicalId":43754,"journal":{"name":"Current Cancer Therapy Reviews","volume":" ","pages":""},"PeriodicalIF":0.6,"publicationDate":"2023-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46807774","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 : 2023-05-02DOI: 10.2174/1573394719666230502110244
Michael A. Renteln
Most existing cancer therapies negatively affect normal tissue as well as cancerous tissue. A potentially effective strategy for treating cancer that precludes off-target damage and could be an option for most patients would involve targeting one or more mutations that are ubiquitous in the given patient’s tumor(s). To effect this strategy, one would employ multi-region sequencing of a patient’s primary tumor and metastases to seek out mutations that are shared between all or at least most regions. Once the target or targets are known, one would ideally rapidly generate a molecular switch for at least one of said ubiquitous mutations that can distinguish the mutated DNA, RNA, or protein from the wild-type version and subsequently trigger a therapeutic response. I propose that the therapeutic response involve the replication of an oncolytic virus or intracellular bacterium, as any mutation can theoretically be detected by a vector that enters the cell - and automatic propagation could be very helpful. Moreover, the mutation “signal” can be easily enhanced through transcriptional and translational (if the target is an intracellular protein) enhancement. Importantly, RNA may make the best target for the molecular switches in terms of amplification of the signal and ease of targeting.
{"title":"Promoting oncolytic vector replication with switches that detect ubiquitous mutations","authors":"Michael A. Renteln","doi":"10.2174/1573394719666230502110244","DOIUrl":"https://doi.org/10.2174/1573394719666230502110244","url":null,"abstract":"\u0000\u0000Most existing cancer therapies negatively affect normal tissue as well as cancerous tissue.\u0000A potentially effective strategy for treating cancer that precludes off-target damage and could be an\u0000option for most patients would involve targeting one or more mutations that are ubiquitous in the\u0000given patient’s tumor(s). To effect this strategy, one would employ multi-region sequencing of a patient’s primary tumor and metastases to seek out mutations that are shared between all or at least\u0000most regions. Once the target or targets are known, one would ideally rapidly generate a molecular\u0000switch for at least one of said ubiquitous mutations that can distinguish the mutated DNA, RNA, or\u0000protein from the wild-type version and subsequently trigger a therapeutic response. I propose that\u0000the therapeutic response involve the replication of an oncolytic virus or intracellular bacterium, as\u0000any mutation can theoretically be detected by a vector that enters the cell - and automatic propagation could be very helpful. Moreover, the mutation “signal” can be easily enhanced through transcriptional and translational (if the target is an intracellular protein) enhancement. Importantly, RNA\u0000may make the best target for the molecular switches in terms of amplification of the signal and ease\u0000of targeting.\u0000","PeriodicalId":43754,"journal":{"name":"Current Cancer Therapy Reviews","volume":" ","pages":""},"PeriodicalIF":0.6,"publicationDate":"2023-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46650004","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 : 2023-05-01DOI: 10.2174/1573394718666220822175032
Aadilah Omar, Paul Ruff, Clement Penny
Background: The Hedgehog (HH) pathway is a key regulator of many important processes in vertebrate embryonic development, including stem cell maintenance, cell differentiation, tissue polarity and cell proliferation. During pathway activation, Ptch no longer inhibits Smo and the full length Gli translocates to the nucleus resulting in the transcription of oncogenes. When constitutively activated, this leads to tumorigenesis in several human cancers. Cyclopamine acts as an antagonist of the HH signalling pathway by directly binding to the Smo heptahelical domain. The involvement of this pathway in metastasis, and its presence in cancer stem cells (CSCs), makes it a valid option for developing a targeted therapeutic against it.
Methods: CSC were isolated from DLD1 and HT29 cell lines using magnetic cell separation labelling the CD133 receptor. The growth patterns of isolated CSCs (CD133 positive) in comparison to non-stem cells (CD133 negative) were analysed using real-time cell impedance assays (RTCA). Thereafter, adhesion, invasion and migration assays were performed with the application of small molecule inhibitors. The expression levels of CD133 and SHH were evaluated using confocal microscopy following treatment with cyclopamine.
Results and Discussion: Growth of CSCs appeared to be slower than non-CSCs. Adhesion, invasion and cell migration were inhibited when CSCs were pharmacologically treated either with cyclopamine or SANT-2 (a synthetic analogue of cyclopamine), small molecule inhibitors of the HH pathway. Using confocal microscopy the cell surface expression of Sonic Hedgehog (SHH) was significantly decreased following treatment with cyclopamine, while the expression of CD133 remained unaffected.
Conclusion: Considering these in vitro results, small molecule inhibitors targeting the SHH pathway appear to be promising therapeutic tools for the treatment of metastatic colon CSCs.
{"title":"Inhibition of the Sonic Hedgehog Pathway using Small Molecule Inhibitors: Targeting Colon Cancer Stem Cells","authors":"Aadilah Omar, Paul Ruff, Clement Penny","doi":"10.2174/1573394718666220822175032","DOIUrl":"https://doi.org/10.2174/1573394718666220822175032","url":null,"abstract":"<p>Background: The Hedgehog (HH) pathway is a key regulator of many important processes in vertebrate embryonic development, including stem cell maintenance, cell differentiation, tissue polarity and cell proliferation. During pathway activation, Ptch no longer inhibits Smo and the full length Gli translocates to the nucleus resulting in the transcription of oncogenes. When constitutively activated, this leads to tumorigenesis in several human cancers. Cyclopamine acts as an antagonist of the HH signalling pathway by directly binding to the Smo heptahelical domain. The involvement of this pathway in metastasis, and its presence in cancer stem cells (CSCs), makes it a valid option for developing a targeted therapeutic against it. <p> Methods: CSC were isolated from DLD1 and HT29 cell lines using magnetic cell separation labelling the CD133 receptor. The growth patterns of isolated CSCs (CD133 positive) in comparison to non-stem cells (CD133 negative) were analysed using real-time cell impedance assays (RTCA). Thereafter, adhesion, invasion and migration assays were performed with the application of small molecule inhibitors. The expression levels of CD133 and SHH were evaluated using confocal microscopy following treatment with cyclopamine. <p> Results and Discussion: Growth of CSCs appeared to be slower than non-CSCs. Adhesion, invasion and cell migration were inhibited when CSCs were pharmacologically treated either with cyclopamine or SANT-2 (a synthetic analogue of cyclopamine), small molecule inhibitors of the HH pathway. Using confocal microscopy the cell surface expression of Sonic Hedgehog (SHH) was significantly decreased following treatment with cyclopamine, while the expression of CD133 remained unaffected. <p> Conclusion: Considering these in vitro results, small molecule inhibitors targeting the SHH pathway appear to be promising therapeutic tools for the treatment of metastatic colon CSCs.</p>","PeriodicalId":43754,"journal":{"name":"Current Cancer Therapy Reviews","volume":"15 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135702907","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 : 2023-05-01DOI: 10.2174/157339471902230210124705
Daniele Santini
{"title":"Meet the Regional Editor","authors":"Daniele Santini","doi":"10.2174/157339471902230210124705","DOIUrl":"https://doi.org/10.2174/157339471902230210124705","url":null,"abstract":"","PeriodicalId":43754,"journal":{"name":"Current Cancer Therapy Reviews","volume":"102 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135801778","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 : 2023-04-27DOI: 10.2174/1573394719666230427094247
H. Borji, Soheil Sadr
Breast cancer is a major cause of cancer deaths in women, with approximately 1.2 million new cases per year. Current treatment options for breast cancer include surgery, radiation, hormone therapy, and chemotherapy. However, the non-selective cytotoxicity of chemotherapeutic agents often leads to severe side effects, while drug resistance can worsen patient outcomes. Therefore, the development of more effective and less toxic anticancer drugs is a critical need. This study aimed to review the literature on Echinococcus granulosus antigens with anticancer potential against triple-negative breast cancer. Recent studies have suggested that certain parasite antigens may have potential anticancer effects. Specifically, research has shown that echinococcosis, a disease caused by the parasitic cestode Echinococcus granulosus, may have a protective effect against cancer. These findings offer new insights into the potential use of E. granulosus antigens in the development of novel cancer therapies and tumor cell vaccines. The findings of recent studies suggested that E. granulosus antigens may have the potential to be used in effective and less toxic cancer treatments. However, further research is needed to fully understand the mechanisms behind the anticancer effects of these antigens and develop new cancer therapies and vaccines
{"title":"Echinococcus granulosus as a Promising Therapeutic Agent against Triplenegative Breast Cancer","authors":"H. Borji, Soheil Sadr","doi":"10.2174/1573394719666230427094247","DOIUrl":"https://doi.org/10.2174/1573394719666230427094247","url":null,"abstract":"\u0000\u0000Breast cancer is a major cause of cancer deaths in women, with approximately 1.2 million\u0000new cases per year. Current treatment options for breast cancer include surgery, radiation, hormone\u0000therapy, and chemotherapy. However, the non-selective cytotoxicity of chemotherapeutic agents often\u0000leads to severe side effects, while drug resistance can worsen patient outcomes. Therefore, the development of more effective and less toxic anticancer drugs is a critical need. This study aimed to review\u0000the literature on Echinococcus granulosus antigens with anticancer potential against triple-negative\u0000breast cancer. Recent studies have suggested that certain parasite antigens may have potential anticancer effects. Specifically, research has shown that echinococcosis, a disease caused by the parasitic\u0000cestode Echinococcus granulosus, may have a protective effect against cancer. These findings offer\u0000new insights into the potential use of E. granulosus antigens in the development of novel cancer therapies and tumor cell vaccines. The findings of recent studies suggested that E. granulosus antigens may\u0000have the potential to be used in effective and less toxic cancer treatments. However, further research is\u0000needed to fully understand the mechanisms behind the anticancer effects of these antigens and develop\u0000new cancer therapies and vaccines\u0000","PeriodicalId":43754,"journal":{"name":"Current Cancer Therapy Reviews","volume":" ","pages":""},"PeriodicalIF":0.6,"publicationDate":"2023-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45867002","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}
Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR/Cas9) technology is currently one of the most promising gene editing techniques. Gene-editing techniques allow various alterations to the DNA sequence by either addition, deletion, or inversion. The two primary components of this technique are the Cas9 endonuclease, which cuts the DNA strands at the specific target position of the genome, and the guide RNA molecule (gRNA), which guides the Cas9 endonuclease to that target portion. This technology is based on the adaptive immune system in prokaryotes, which prevents the entry of viruses by integrating short virus sequences in the cell’s CRISPR locus and allowing it to remember, recognize, and clear infections. The use of CRISPR technology in cancer biology is evolving quickly and holds great promise for the development of cancer models, blocking drug resistance, screening functional genes, gene editing, and CAR T cell therapy
{"title":"CRISPR/Cas9’s Major Role in Revolutionizing the Field of Cancer","authors":"Ankit Sharma, Agrata Singh, Khushi Sharma, Uzma Abdulbaseer, Estevan Ruiz Limon Lopez","doi":"10.2174/1573394719666230426152155","DOIUrl":"https://doi.org/10.2174/1573394719666230426152155","url":null,"abstract":"\u0000\u0000Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR/Cas9) technology is\u0000currently one of the most promising gene editing techniques. Gene-editing techniques allow various\u0000alterations to the DNA sequence by either addition, deletion, or inversion. The two primary components\u0000of this technique are the Cas9 endonuclease, which cuts the DNA strands at the specific target position\u0000of the genome, and the guide RNA molecule (gRNA), which guides the Cas9 endonuclease to that target portion. This technology is based on the adaptive immune system in prokaryotes, which prevents\u0000the entry of viruses by integrating short virus sequences in the cell’s CRISPR locus and allowing it to\u0000remember, recognize, and clear infections. The use of CRISPR technology in cancer biology is evolving quickly and holds great promise for the development of cancer models, blocking drug resistance,\u0000screening functional genes, gene editing, and CAR T cell therapy\u0000","PeriodicalId":43754,"journal":{"name":"Current Cancer Therapy Reviews","volume":" ","pages":""},"PeriodicalIF":0.6,"publicationDate":"2023-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42447172","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 : 2023-04-26DOI: 10.2174/1573394719666230426151557
H. Abdullah, Syahirah Sazeli, Norlida Mamat, Hermizi Hapidin, S. Sulong
Most cervical cancer fatalities have been reported due to drug resistance, invasion, and metastasis. Combination therapy is a prominent technique for overcoming the toxicity of cancer chemotherapy to normal cells, which is mediated across numerous targeted pathways and requires a lower dose of each individual agent. Polyphenolic substances have the potential to improve chemotherapy efficacy while also reducing negative effects. This study aimed to review the research findings on the role of reactive oxygen species (ROS) in cervical cancer cell HeLa treated with combination therapy. Hydroxyl radicals damage DNA, causing a cascade of structural changes in purine and pyrimidine bases that could lead to mutagenicity. ROS, such as hydroxyl radical (OH- ), superoxide anions (O2 - ), hydrogen peroxide (H2O2), and peroxyl radicals (ROO- ), are frequent products of aerobic metabolism that can be beneficial or detrimental to the biological system. To combat the harmful effects of ROS, cells have an antioxidative defense system that comprises superoxide dismutases, catalase, glutathione, and other defensive mechanisms. Excessive ROS accumulation causes DNA damage, which triggers the apoptotic machinery, resulting in cell death. Chemotherapeutic medications with phenolic compounds or polyphenol-rich extracts exhibit anticancer synergy. Combination treatment with polyphenols and anticancer drugs is one of the promising approaches in the treatment of cervical cancer.
{"title":"ROS Modulate Cell Death Mechanism in Cervical Cancer Cells Treated\u0000with the Combination of Polyphenolic Compounds and Anticancer Drug\u0000Cisplatin: A Review","authors":"H. Abdullah, Syahirah Sazeli, Norlida Mamat, Hermizi Hapidin, S. Sulong","doi":"10.2174/1573394719666230426151557","DOIUrl":"https://doi.org/10.2174/1573394719666230426151557","url":null,"abstract":"Most cervical cancer fatalities have been reported due to drug resistance, invasion, and metastasis. Combination therapy is a prominent technique for overcoming the toxicity of cancer chemotherapy to normal cells, which is mediated across numerous targeted pathways and requires a\u0000lower dose of each individual agent. Polyphenolic substances have the potential to improve chemotherapy efficacy while also reducing negative effects.\u0000\u0000\u0000\u0000This study aimed to review the research findings on the role of reactive oxygen species (ROS) in\u0000cervical cancer cell HeLa treated with combination therapy.\u0000\u0000\u0000\u0000Hydroxyl radicals damage DNA, causing a cascade of structural changes in purine and pyrimidine bases that could lead to mutagenicity. ROS, such as hydroxyl radical (OH-\u0000), superoxide anions (O2\u0000-\u0000),\u0000hydrogen peroxide (H2O2), and peroxyl radicals (ROO-\u0000), are frequent products of aerobic metabolism\u0000that can be beneficial or detrimental to the biological system. To combat the harmful effects of ROS,\u0000cells have an antioxidative defense system that comprises superoxide dismutases, catalase, glutathione,\u0000and other defensive mechanisms. Excessive ROS accumulation causes DNA damage, which triggers\u0000the apoptotic machinery, resulting in cell death.\u0000\u0000\u0000\u0000Chemotherapeutic medications with phenolic compounds or polyphenol-rich extracts exhibit anticancer synergy. Combination treatment with polyphenols and anticancer drugs is one of the\u0000promising approaches in the treatment of cervical cancer.","PeriodicalId":43754,"journal":{"name":"Current Cancer Therapy Reviews","volume":" ","pages":""},"PeriodicalIF":0.6,"publicationDate":"2023-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42581710","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}