Pub Date : 2022-01-01DOI: 10.1080/23723556.2022.2078628
Ma de Lourdes Zuñiga Martinez, Carlos Miguel López Mendoza, Jared Tenorio Salazar, Alejandro Manuel García Carrancá, Marco Antonio Cerbón Cervantes, Luz Eugenia Alcántara-Quintana
Cell lines have been considered excellent research models in many areas of biomedicine and, specifically, in the study of carcinogenesis. However, they cease to be effective models if their behavior changes. Although studies on the cross-contamination of cell lines originating from different tissues have been performed, little is known about cell lines derived from cervical neoplasia. We know that high-risk HPV (HR-HPV) is associated with the development of this type of cancer. This link between HPV infection and cancer was first established over 35 years ago when HPV16 DNA was found to be present in a large proportion of cervical cancer biopsies. The present review paper aims to report the status of the establishment, authenticity, and characterization of cervical cancer (CC) cell lines. This is a systematic review of articles on the establishment, authenticity, and characterization of CC cell lines, published from 1960 to date in the databases and in cell repository databases. 52 cell lines were identified in the literature. Only 25 cell lines were derived from cervical neoplasia, of which only 45.8% have a reported identity test (genomic fingerprint). Despite the increase in the establishment of cell lines of cervical neoplasia and the standards for the regulation of these study models, the criteria for their characterization continue to be diverse.
{"title":"Establishment, authenticity, and characterization of cervical cancer cell lines.","authors":"Ma de Lourdes Zuñiga Martinez, Carlos Miguel López Mendoza, Jared Tenorio Salazar, Alejandro Manuel García Carrancá, Marco Antonio Cerbón Cervantes, Luz Eugenia Alcántara-Quintana","doi":"10.1080/23723556.2022.2078628","DOIUrl":"https://doi.org/10.1080/23723556.2022.2078628","url":null,"abstract":"<p><p>Cell lines have been considered excellent research models in many areas of biomedicine and, specifically, in the study of carcinogenesis. However, they cease to be effective models if their behavior changes. Although studies on the cross-contamination of cell lines originating from different tissues have been performed, little is known about cell lines derived from cervical neoplasia. We know that high-risk HPV (HR-HPV) is associated with the development of this type of cancer. This link between HPV infection and cancer was first established over 35 years ago when HPV16 DNA was found to be present in a large proportion of cervical cancer biopsies. The present review paper aims to report the status of the establishment, authenticity, and characterization of cervical cancer (CC) cell lines. This is a systematic review of articles on the establishment, authenticity, and characterization of CC cell lines, published from 1960 to date in the databases and in cell repository databases. 52 cell lines were identified in the literature. Only 25 cell lines were derived from cervical neoplasia, of which only 45.8% have a reported identity test (genomic fingerprint). Despite the increase in the establishment of cell lines of cervical neoplasia and the standards for the regulation of these study models, the criteria for their characterization continue to be diverse.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"9 1","pages":"2078628"},"PeriodicalIF":2.1,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9176225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10432933","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}
Pub Date : 2021-11-16DOI: 10.1080/23723556.2021.2000318
Amanda K Riley, Alice H Berger
In recent work, we performed CRISPR/Cas9 screening in RIT1 (Ras-like in all tissues)-mutant cancer cells. We found that RIT1-mutant cells are vulnerable to loss of mitotic regulators, and mutant RIT1 synergizes with YAP1 (yes-associated protein 1) in oncogenesis. These findings can be leveraged to identify targeted therapies for RIT1-mutant cancer.
{"title":"Genome-wide CRISPR screening reveals novel therapeutic targets in RIT1-driven lung cancer.","authors":"Amanda K Riley, Alice H Berger","doi":"10.1080/23723556.2021.2000318","DOIUrl":"https://doi.org/10.1080/23723556.2021.2000318","url":null,"abstract":"<p><p>In recent work, we performed CRISPR/Cas9 screening in <i>RIT1 (Ras-like in all tissues)-</i>mutant cancer cells. We found that <i>RIT1</i>-mutant cells are vulnerable to loss of mitotic regulators, and mutant RIT1 synergizes with YAP1 (yes-associated protein 1) in oncogenesis. These findings can be leveraged to identify targeted therapies for <i>RIT1</i>-mutant cancer.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 6","pages":"2000318"},"PeriodicalIF":2.1,"publicationDate":"2021-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8997261/pdf/KMCO_8_2000318.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41145264","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}
Pub Date : 2021-11-09eCollection Date: 2021-01-01DOI: 10.1080/23723556.2021.1997040
Bi Shi, Wei Li, Hao Jiang
Alterations of epigenetic modulators are extensively associated with cancer, but their key molecular activities in cancer regulation are often unclear. We discovered that lysine demethylase 6A (KDM6A, also known as UTX) suppresses cancer by forming liquid-like condensates with lysine methyltransferase 2D (KMT2D, also known as MLL4) and regulating chromatin activity at multiple levels.
{"title":"Epigenetic condensates regulate chromatin activity and tumorigenesis.","authors":"Bi Shi, Wei Li, Hao Jiang","doi":"10.1080/23723556.2021.1997040","DOIUrl":"https://doi.org/10.1080/23723556.2021.1997040","url":null,"abstract":"<p><p>Alterations of epigenetic modulators are extensively associated with cancer, but their key molecular activities in cancer regulation are often unclear. We discovered that lysine demethylase 6A (KDM6A, also known as UTX) suppresses cancer by forming liquid-like condensates with lysine methyltransferase 2D (KMT2D, also known as MLL4) and regulating chromatin activity at multiple levels.</p>","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":"8 5","pages":"1997040"},"PeriodicalIF":2.1,"publicationDate":"2021-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/6f/d8/KMCO_8_1997040.PMC8632315.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39688332","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}
Pub Date : 2021-11-02DOI: 10.1080/23723556.2021.1989262
Yuan Zhu, Wang Zheng, Emmanuelle S. Jecrois, Brianna R. Pierce, Daniel M. Treisman
ABSTRACT Pediatric low-grade gliomas (pLGGs) are almost universally driven by abnormal activation of RAS-mediated MEK-ERK/MAPK signaling pathway. pLGGs predominantly occur in children, suggesting that they originate in an ERK-dependent neural stem/progenitor population(s) transiently present in the developing brain. Our recent preclinical study reveals a cell-lineage-of-origin and develops a chemopreventative therapeutic strategy.
{"title":"A therapeutic window for preventive therapy in NF1-associated optic pathway glioma","authors":"Yuan Zhu, Wang Zheng, Emmanuelle S. Jecrois, Brianna R. Pierce, Daniel M. Treisman","doi":"10.1080/23723556.2021.1989262","DOIUrl":"https://doi.org/10.1080/23723556.2021.1989262","url":null,"abstract":"ABSTRACT Pediatric low-grade gliomas (pLGGs) are almost universally driven by abnormal activation of RAS-mediated MEK-ERK/MAPK signaling pathway. pLGGs predominantly occur in children, suggesting that they originate in an ERK-dependent neural stem/progenitor population(s) transiently present in the developing brain. Our recent preclinical study reveals a cell-lineage-of-origin and develops a chemopreventative therapeutic strategy.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44070503","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 : 2021-11-02DOI: 10.1080/23723556.2021.1997331
S. Fröhling
ABSTRACT For most rare cancers, precision oncology approaches are not established because these entities are poorly understood and their investigation requires the collaboration of many centers. The MASTER precision oncology network demonstrates that clinical whole-genome/exome and RNA sequencing yield molecular mechanism-aware treatments that benefit a substantial proportion of patients with advanced rare cancers and will prepare the ground for future clinical trials.
{"title":"Interdisciplinary team science to understand and intercept rare cancers","authors":"S. Fröhling","doi":"10.1080/23723556.2021.1997331","DOIUrl":"https://doi.org/10.1080/23723556.2021.1997331","url":null,"abstract":"ABSTRACT For most rare cancers, precision oncology approaches are not established because these entities are poorly understood and their investigation requires the collaboration of many centers. The MASTER precision oncology network demonstrates that clinical whole-genome/exome and RNA sequencing yield molecular mechanism-aware treatments that benefit a substantial proportion of patients with advanced rare cancers and will prepare the ground for future clinical trials.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47283118","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 : 2021-11-02DOI: 10.1080/23723556.2021.2009423
Caiyun Liu, Xinjian Li
ABSTRACT How cancer cells absorb enough glucose to support their rapid growth is poorly understood. We have recently demonstrated that palmitoyl transferase DHHC9 palmitoylates glucose transporter GLUT1 at Cys207 to maintain GLUT1 plasma membrane localization. DHHC9-mediated GLUT1 palmitoylation supports glycolysis, proliferation, colony formation, and tumorigenicity of glioblastoma cells.
{"title":"Greasy GLUT1 maintains glioblastoma malignancy","authors":"Caiyun Liu, Xinjian Li","doi":"10.1080/23723556.2021.2009423","DOIUrl":"https://doi.org/10.1080/23723556.2021.2009423","url":null,"abstract":"ABSTRACT How cancer cells absorb enough glucose to support their rapid growth is poorly understood. We have recently demonstrated that palmitoyl transferase DHHC9 palmitoylates glucose transporter GLUT1 at Cys207 to maintain GLUT1 plasma membrane localization. DHHC9-mediated GLUT1 palmitoylation supports glycolysis, proliferation, colony formation, and tumorigenicity of glioblastoma cells.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42374549","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 : 2021-11-02DOI: 10.1080/23723556.2021.2002120
C. G. Langdon, M. Hatley
ABSTRACT Fusion-negative rhabdomyosarcoma (FN-RMS) is molecularly heterogeneous with few universal alterations except for Phosphatase and tensin homolog (PTEN) promoter hypermethylation. We demonstrate that losing Pten in FN-RMS engages an aberrant transcriptional program key in tumor maintenance and cell identity. These results highlight the importance between transcriptional state, cell of origin, and genetic perturbation in tumorigenesis.
{"title":"The perfect PTEN – transcriptional regulation by PTEN dictates sarcoma identity","authors":"C. G. Langdon, M. Hatley","doi":"10.1080/23723556.2021.2002120","DOIUrl":"https://doi.org/10.1080/23723556.2021.2002120","url":null,"abstract":"ABSTRACT Fusion-negative rhabdomyosarcoma (FN-RMS) is molecularly heterogeneous with few universal alterations except for Phosphatase and tensin homolog (PTEN) promoter hypermethylation. We demonstrate that losing Pten in FN-RMS engages an aberrant transcriptional program key in tumor maintenance and cell identity. These results highlight the importance between transcriptional state, cell of origin, and genetic perturbation in tumorigenesis.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43439788","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 : 2021-11-02DOI: 10.1080/23723556.2021.1985930
Romain Villot, Audrey Poirier, R. Devillers, A. Kolnoguz, S. Elowe, V. Manem, P. Joubert, Frédérick A. Mallette, M. Laplante
ABSTRACT We recently identified Zinc-finger protein 768 (ZNF768) as a novel transcription factor controlling cell fate decision downstream of Rat sarcoma virus (RAS). We showed that ZNF768 depletion impairs cell cycle progression and triggers cellular senescence, while its overexpression allows cells to bypass oncogene-induced senescence. Elevated ZNF768 levels is common in tumors, suggesting that ZNF768 may help to escape cellular senescence, sustain proliferation and promote malignant transformation. Here, we discuss these recent findings and highlight key questions emerging from our work.
{"title":"ZNF768: controlling cellular senescence and proliferation with ten fingers","authors":"Romain Villot, Audrey Poirier, R. Devillers, A. Kolnoguz, S. Elowe, V. Manem, P. Joubert, Frédérick A. Mallette, M. Laplante","doi":"10.1080/23723556.2021.1985930","DOIUrl":"https://doi.org/10.1080/23723556.2021.1985930","url":null,"abstract":"ABSTRACT We recently identified Zinc-finger protein 768 (ZNF768) as a novel transcription factor controlling cell fate decision downstream of Rat sarcoma virus (RAS). We showed that ZNF768 depletion impairs cell cycle progression and triggers cellular senescence, while its overexpression allows cells to bypass oncogene-induced senescence. Elevated ZNF768 levels is common in tumors, suggesting that ZNF768 may help to escape cellular senescence, sustain proliferation and promote malignant transformation. Here, we discuss these recent findings and highlight key questions emerging from our work.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46161742","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 : 2021-11-02DOI: 10.1080/23723556.2021.2010512
Mariana Paes Dias, J. Jonkers
ABSTRACT Tumors with loss of breast cancer type 1 susceptibility protein (BRCA1) are homologous recombination (HR) deficient and hypersensitive to poly(ADP-ribose) polymerase inhibitors (PARPi). However, these tumors may restore HR and acquire PARPi resistance via loss of end-protection of DNA double-strand breaks. We found that loss of nuclear DNA ligase III resensitizes HR-restored BRCA1-deficient cells to PARPi by exposing post-replicative single-stranded DNA (ssDNA) gaps. Our work, and that of others, identifies ssDNA gaps as a key determinant of PARPi response.
{"title":"Filling in the gaps in PARP inhibitor-induced synthetic lethality","authors":"Mariana Paes Dias, J. Jonkers","doi":"10.1080/23723556.2021.2010512","DOIUrl":"https://doi.org/10.1080/23723556.2021.2010512","url":null,"abstract":"ABSTRACT Tumors with loss of breast cancer type 1 susceptibility protein (BRCA1) are homologous recombination (HR) deficient and hypersensitive to poly(ADP-ribose) polymerase inhibitors (PARPi). However, these tumors may restore HR and acquire PARPi resistance via loss of end-protection of DNA double-strand breaks. We found that loss of nuclear DNA ligase III resensitizes HR-restored BRCA1-deficient cells to PARPi by exposing post-replicative single-stranded DNA (ssDNA) gaps. Our work, and that of others, identifies ssDNA gaps as a key determinant of PARPi response.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46061335","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 : 2021-11-02DOI: 10.1080/23723556.2021.2013723
Mariana Cooke
ABSTRACT In a recent study, our group identified RAC guanine nucleotide exchange factors (RAC-GEFs) driving motility signaling in KRAS mutant lung adenocarcinoma cells. The RAC-GEFs FARP1, ARHGEF39 and TIAM2 play fundamental roles in the formation of membrane ruffles in response to growth factor receptor stimulation.
{"title":"Novel insights into the RTK-dependent metastatic phenotype of KRAS-mutant lung adenocarcinoma","authors":"Mariana Cooke","doi":"10.1080/23723556.2021.2013723","DOIUrl":"https://doi.org/10.1080/23723556.2021.2013723","url":null,"abstract":"ABSTRACT In a recent study, our group identified RAC guanine nucleotide exchange factors (RAC-GEFs) driving motility signaling in KRAS mutant lung adenocarcinoma cells. The RAC-GEFs FARP1, ARHGEF39 and TIAM2 play fundamental roles in the formation of membrane ruffles in response to growth factor receptor stimulation.","PeriodicalId":37292,"journal":{"name":"Molecular and Cellular Oncology","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2021-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49485087","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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