Identity tests: determination of cell line cross-contamination

Cabrera, Carmen; Cobo, Fernando; Nieto, Ana; Cortés, José Luis; Montes, Rosa; Catalina, Purificación; Concha, Ángel

doi:10.1007/s10616-006-9013-8

Cited by 42 publications

(22 citation statements)

References 27 publications

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“…Chang (National Taiwan University, Taipei, Taiwan) in 2012 (18). These cell lines have been tested and authenticated according to the published guidelines before the study initiation (19). The TW1.5, TW2.6, Hep2, and SCC9 were cultured in DMEM/F12 (Gibco).…”

Section: Cell Culture and Establishment Of Cisplatin-resistant Cell Lmentioning

confidence: 99%

Histone Methyltransferase G9a Drives Chemotherapy Resistance by Regulating the Glutamate–Cysteine Ligase Catalytic Subunit in Head and Neck Squamous Cell Carcinoma

Liu

Hua

et al. 2017

Molecular Cancer Therapeutics

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Transient chemotherapeutic response is a major obstacle to treating head and neck squamous cell carcinomas (HNSCC). Histone methyltransferase G9a has recently been shown to be abundantly expressed in HNSCC, and is required to maintain the malignant phenotype. In this study, we found that high G9a expression is significantly associated with poor chemotherapeutic response and disease-free survival in HNSCC patients. Similarly, G9a expression and enzymatic activity were elevated in cisplatinresistant HNSCC cells. Genetic or pharmacologic inhibition of G9a sensitized the resistant cells to cisplatin, increasing cellular apoptosis. Mechanistic investigations indicated that G9a contributes to transcriptional activation of the glutamate-cysteine ligase catalytic subunit (GCLC), which results in upregulation of cellular glutathione (GSH) and drug resistance. In addition, we observed a significant positive correlation between G9a and GCLC expression in tumors of HNSCC patients. Taken together, our findings provide evidence that G9a protects HNSCC cells against chemotherapy by increasing the synthesis of GSH, and imply G9a as a promising target for overcoming cisplatin resistance in HNSCC.

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Section: Cell Culture and Establishment Of Cisplatin-resistant Cell Lmentioning

confidence: 99%

Histone Methyltransferase G9a Drives Chemotherapy Resistance by Regulating the Glutamate–Cysteine Ligase Catalytic Subunit in Head and Neck Squamous Cell Carcinoma

Liu

Hua

et al. 2017

Molecular Cancer Therapeutics

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“…These cell lines have been tested and authenticated according to the published guideline before the initiation of the study (18). The pcDNA3-Snail was generated by insertion of a 795 bp fragment of the full-length human Snail cDNA into the HindIII/EcoRI sites of the pcDNA3.1 vector.…”

Section: Analysis Of Microarray Expression Datasetsmentioning

confidence: 99%

Regulation of Excision Repair Cross-Complementation Group 1 by Snail Contributes to Cisplatin Resistance in Head and Neck Cancer

Hsu

Lan

Huang

et al. 2010

Clinical Cancer Research

133

108

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Purpose: We investigated the mechanism and clinical significance of the epithelial-mesenchymal transition (EMT)-induced chemoresistance in head and neck squamous cell carcinoma (HNSCC).Experimental Design: The correlation between the expression of different EMT regulators and chemoresistance genes, such as excision repair cross complementation group 1 (ERCC1), was evaluated in cancer cell lines from the NCI-60 database and four human HNSCC cell lines. Ectopic expression of Snail or short-interference RNA-mediated repression of Snail or ERCC1 was done in HNSCC cell lines. Cell viability was examined for cells after cisplatin treatment. A luciferase reporter assay and chromatin immunoprecipitation were used to identify the transcriptional regulation of ERCC1 by Snail. Immunohistochemical analysis of Snail, Twist1, ERCC1, hypoxia inducible factor-1 α (HIF-1α), and NBS1 were done in samples from 72 HNSCC patients receiving cisplatin-based chemotherapy.Results: The correlation between the expression of Snail and ERCC1 was confirmed in different cell lines, including HNSCC cells. In HNSCC cell lines, overexpression of Snail in the low endogenous Snail/ ERCC1 cell lines FaDu or CAL-27 increased ERCC1 expression, and hypoxia or overexpression of NBS1 also upregulated ERCC1. Knockdown of Snail in the high endogenous Snail/ERCC1 cell line OECM-1 downregulated ERCC1 expression and attenuated cisplatin resistance. Furthermore, suppression of ERCC1 in Snail-or NBS1-overexpressing HNSCC cells enhanced sensitivity to cisplatin. Snail directly regulated ERCC1 transcription. In patients with HNSCC, coexpression of Snail and ERCC1 correlated with cisplatin resistance and a poor prognosis.Conclusions: Activation of ERCC1 by Snail is critical in the generation of cisplatin resistance of HNSCC cells. Clin Cancer Res; 16(18); 4561-71. ©2010 AACR.The epithelial-mesenchymal transition (EMT), a major mechanism of cancer metastasis, is initiated by repression of the epithelial adhesion molecule E-cadherin by several transcription factors, including Snail (also known as Snail1), Slug (also known as Snail2), Twist1, Zeb1, SIP1, and E47 (1). In most human cancers, metastatic tumors are resistant to chemotherapy; therefore, patients with such tumors typically have poor outcomes. Emerging evidence suggests a correlation between EMT and the resistance to chemotherapy of cancer cells. For example, colorectal cancer cells that are resistant to oxaliplatin undergo phenotypic changes indicative of an EMT (2). Direct regulation of Akt2 by Twist contributes to paclitaxel resistance in breast cancer cells (3). Induction of EMT in breast cancer cells leads to an enrichment of cells with stem-like properties and chemoresistance (4). A recent report found that Zeb1 and other EMT regulators allow pancreatic cancer cells to maintain drug resistance (5). Taken together, these studies suggest that diverse types of cancer cells acquire drug-resistant phenotypes during EMT. Although there is an evident association among EMT, metastasis, and chemoresis...

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“…The aberrant chromosome number suggested the malignant phenotype of these cells. In addition, the STR profiling of each cell line were tested to avoid the possibility of cell line cross-contamination (27,28). The data of the 8 core loci (Table Ⅰ) were searched in ATCC and DSMZ STR databank and did not return any similar results.…”

Section: Establishment Of Pda Cell Lines and Characterizationmentioning

confidence: 99%

Intrinsic gemcitabine resistance in a novel pancreatic cancer cell line is associated with cancer stem cell-like phenotype

Fu²,

Ouyang³

et al. 2011

Int J Oncol

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Abstract. Pancreatic ductal adenocarcinoma (PDA) remains one of the most lethal malignancies in the world, often diagnosed at an advanced stage, resistant to conventional chemotherapy and having high invasive and metastatic potential. The mechanism of drug resistance of PDA is still not clear. In the present study, we established two novel pancreatic cancer cell lines PAXC-002 and PAXC-003 from human primary xenograft models. The cell lines were characterized by morphology, karyotype, pancreatic cancer marker and short tandem repeat (STR) analysis, and growth kinetics and tumorigenicity. The in vitro anti-proliferation test revealed that PAXC-002 cell was intrinsically resistant to the standard of care chemotherapy-gemcitabine, compared with that of PAXC-003 and other widely used pancreatic cancer cell lines. Interestingly, the gemcitabine resistant PAXC-002 cell line was more potent in forming colonies in 3-Dimensional matrigel culture conditions and had a higher percentage of CD133 positive cells, which is recognized as a cancer stem cell marker, compared to the gemcitabine-sensitive PAXC-003 cell line. In this study, we present two novel pancreatic cancer cell lines which could be used for gemcitabine resistance investigation, mechanism identification of pancreatic cancer and anticancer drug screening. The preliminary data indicate that the drug resistance of pancreatic carcinoma cells is associated with a cancer stem cell-like phenotype.

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Identity tests: determination of cell line cross-contamination

Cited by 42 publications

References 27 publications

Histone Methyltransferase G9a Drives Chemotherapy Resistance by Regulating the Glutamate–Cysteine Ligase Catalytic Subunit in Head and Neck Squamous Cell Carcinoma

Histone Methyltransferase G9a Drives Chemotherapy Resistance by Regulating the Glutamate–Cysteine Ligase Catalytic Subunit in Head and Neck Squamous Cell Carcinoma

Regulation of Excision Repair Cross-Complementation Group 1 by Snail Contributes to Cisplatin Resistance in Head and Neck Cancer

Intrinsic gemcitabine resistance in a novel pancreatic cancer cell line is associated with cancer stem cell-like phenotype

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