Establishment and characterization of a poorly differentiated lethal human endometrial carcinoma cell line (NOU-1) with karyotype 46,XX

Faruqi, Shamim A.; Satyaswaroop, P.G.; LiVolsi, Virginia A.; Deger, Randolph B.; Noumoff, Joel S.

doi:10.1016/s0165-4608(01)00658-6

Cited by 4 publications

(4 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These observations provide evidence to suggest that these cell lines represent a useful model for in vitro studies testing therapeutic approaches for type I (endometrioid) endometrial cancers. In addition, there is also evidence that these cell lines recapitulate the properties of human endometrial cancers in xenograft studies (48,49).…”

Section: Discussionmentioning

confidence: 97%

PTEN Deficiency in Endometrioid Endometrial Adenocarcinomas Predicts Sensitivity to PARP Inhibitors

et al. 2010

View full text Add to dashboard Cite

PTEN (phosphatase and tensin homolog) loss of function is the most common genetic aberration in endometrioid endometrial carcinomas. In addition to its well-described role in cell signaling, PTEN is involved in the maintenance of genomic stability. Loss of PTEN function causes defects in repair of DNA double-strand breaks by homologous recombination and, therefore, sensitizes cells to inhibition of the poly(adenosine diphosphate ribose) polymerase (PARP). Here, we determined the PTEN status of eight endometrioid endometrial carcinoma cell lines and correlated it with in vitro sensitivity to the PARP inhibitor KU0058948. PTEN-deficient cells showed a significantly greater sensitivity to KU0058948 than the two endometrioid endometrial carcinoma cell lines with wild-type PTEN. The cell lines lacking PTEN expression were unable to elicit a homologous recombination damage response as assayed by RAD51 focus function (a marker of competent homologous recombination DNA repair) upon irradiation and treatment with PARP inhibitors. PTEN silencing in PTEN wild-type Hec-1b cells resulted in reduced RAD51 foci formation after DNA damage and increased sensitivity to PARP inhibition. PTEN reexpression in PTEN-null cell lines resulted in enhanced RAD51 foci formation and in relative resistance to KU0058948. Given that up to 80% of endometrioid endometrial cancers lack PTEN expression, our results suggest that PARP inhibitors may be therapeutically useful for a subset of endometrioid endometrial cancers.

show abstract

Section: Discussionmentioning

confidence: 97%

PTEN Deficiency in Endometrioid Endometrial Adenocarcinomas Predicts Sensitivity to PARP Inhibitors

et al. 2010

View full text Add to dashboard Cite

show abstract

“…To interrogate the functional relevance of GPC5 in sarcomatous transformation, a plasmid construct carrying the coding sequence of GPC5 gene, under a constitutive promoter, was transfected into NOU‐1 cells, initially derived from a poorly differentiated endometrial carcinoma . Expression of the construct was verified by immunoblot.…”

Section: Resultsmentioning

confidence: 99%

Genomic profiling identifies GPC5 amplification in association with sarcomatous transformation in a subset of uterine carcinosarcomas

Chui

Have

Hoang

et al. 2018

The Journal of Pathology CR

View full text Add to dashboard Cite

Uterine carcinosarcoma, also known as Malignant Mixed Müllerian Tumour, is a high‐grade biphasic neoplasm composed of sarcomatous elements thought to originate via transdifferentiation from high‐grade endometrial carcinoma. To identify molecular factors contributing to the histogenesis of this tumour, we analyzed DNA extracted from matched carcinoma and sarcoma components from 12 cases of carcinosarcoma by a molecular inversion probe microarray to assess genomic copy number alterations (CNAs) and allelic imbalances. Widespread CNAs were identified in tumours with serous histology in the carcinoma component (9/12), while the remaining three cases with endometrioid carcinoma were near‐diploid. Quantification of the extent of genomic aberrations revealed a significant increase in sarcoma relative to carcinoma in tumours with well‐delineated histologic components. Focal amplification of 13q31.3 was identified in 6/12 profiled tumours, of which four harboured the aberration exclusively in the sarcoma component. This result was verified by fluorescence in situ hybridization against GPC5, the only gene situated within the minimal region of amplification. In a validation cohort composed of 97 carcinosarcomas and other uterine sarcomas, amplification of GPC5 (GPC5/CEP13 ratio ≥ 2.2) was identified in 11/97 (11.3%) cases (9/64 carcinosarcoma, 1/3 rhabdomyosarcoma, 1/21 leiomyosarcoma, 0/8 adenosarcoma, 0/1 undifferentiated endometrial sarcoma) and an additional 4 (2.8%) cases had low level gains (GPC5/CEP13 ratio ≥1.5 but <2.2). The functional relevance of Glypican‐5, the gene product of GPC5, in regulating differentiation and lineage commitment was demonstrated in an endometrial carcinoma cell line in vitro. In conclusion, we identified GPC5 amplification as a molecular event mediating epithelial‐mesenchymal transdifferentiation in a subset of uterine carcinosarcomas.

show abstract

“…Despite the cell lines may only present a part of the characteristics of the tumor19, it is still necessary to establish novel and well-characterized EC cell lines to investigate the mechanism of genesis and development, and then so as to develop new therapies against cancer. Many adenocarcinoma cell lines derived from human endometrial tissue have been applied to experimental research8-15. In this literature, we established a new human endometrioid adenocarcinoma cell line, designated ZJB-ENC1.…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, disease-orientated drug screening using human tumor cell lines in vitro has some predictive value for the activity of clinical responses6, 7. To date, despite a number of endometrial carcinoma cell lines have been reported8-15, few originated from poorly differentiated endometrioid adenocarcinoma. Therefore, it is absolutely necessary to establish stable and available cell lines of endometrioid adenocarcinoma.…”

Section: Introductionmentioning

confidence: 99%

Establishment and characterization of novel human primary endometrial cancer cell line (ZJB-ENC1) and its genomic characteristic

Liu

Ren

et al. 2019

J. Cancer

View full text Add to dashboard Cite

The establishment of human malignant tumor cell lines can provide abundant experimental materials for understanding the biological characteristics of tumors, studying the carcinogenesis, molecular genetics and the mechanism of metastasis and evolution. In this study, a novel cell line designated ZJB-ENC1 has been established from poorly differentiated endometrioid adenocarcinoma. Cytological results showed monolayer-cultured cells were polygonal in shape and a piling-up tendency without contact inhabitation. Immunohistochemistry analysis showed that the cells were negative for ER, PR, c-erbB2, E-CAD, CD117, and OCT3/4, but strongly positive for PTEN and P16. Meanwhile, the tumorigenicity of ZJB-ENC1 was confirmed by subcutaneous transplantation of the cells into a xenograft mouse model. In addition, the results of the whole exome sequencing revealed a unique genomic characteristic of ZJB-ENC1 cells, all common and novel SNPs and InDels were identified. In conclusion, this new stable cell line may promote basic and clinical research on endometrial cancer (EC).

show abstract

Establishment and characterization of a poorly differentiated lethal human endometrial carcinoma cell line (NOU-1) with karyotype 46,XX

Cited by 4 publications

References 26 publications

PTEN Deficiency in Endometrioid Endometrial Adenocarcinomas Predicts Sensitivity to PARP Inhibitors

PTEN Deficiency in Endometrioid Endometrial Adenocarcinomas Predicts Sensitivity to PARP Inhibitors

Genomic profiling identifies GPC5 amplification in association with sarcomatous transformation in a subset of uterine carcinosarcomas

Establishment and characterization of novel human primary endometrial cancer cell line (ZJB-ENC1) and its genomic characteristic

Contact Info

Product

Resources

About