Chemotherapy for advanced, recurrent or metastatic endometrial carcinoma

Humber, C.; Tierney, Jayne; Symonds, Paul; Collingwood, M; Kirwan, John; Williams, Chris; Green, J

doi:10.1002/14651858.cd003915.pub2

Cited by 21 publications

(12 citation statements)

References 76 publications

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“…2,3 Although various therapies for treating EC have been improved, the therapeutic effects remain disillusionary. 4,5 In consequence, further molecular researches on the potential mechanism of EC to explore promising therapeutic targets in EC are the urgent problems to be solved.…”

Section: Introductionmentioning

confidence: 99%

<p>Silencing of Long Non-Coding RNA LINC01106 Suppresses the Proliferation, Migration and Invasion of Endometrial Cancer Cells Through Regulating the miR-449a/MET Axis</p>

Gao¹,

Yu²,

Zhang³

et al. 2020

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Endometrial cancer (EC) is an aggressive tumor in females and the development of EC is considered to regulate by some long non-coding RNAs (lncRNAs). Therefore, this study aimed to investigate the regulatory mechanism of lncRNA LINC01106 on EC. Methods: The expression of lncRNA LINC01106, miR-449a and MET in EC tissues and cells was detected by qRT-PCR. Through MTT, wound healing and transwell invasion assays, the proliferation, migration and invasion of EC cells were detected, respectively. The xenograft tumor model was constructed in nude mice to confirm the inhibiting effect of LINC01106 knockdown on EC in vivo. The interactions between miR-449a and LINC01106/ MET were predicted by Starbase/Targetscan software and verified by the dual-luciferase reporter assay or RNA immunoprecipitation assay. Western blot assay was performed to determine the protein level of MET. Results: LncRNA LINC01106 expression was highly up-regulated in EC tissues and cells. The proliferation, migration and invasion of EC cells in vitro were inhibited by the transfection of sh-LINC01106. The growth of tumor xenograft was suppressed by injection of sh-LINC01106. MiR-449a was a target of LINC01106and was negatively modulated by LINC01106. MiR-449a overexpression suppressed the proliferation, migration and invasion of EC cells. In addition, MET was identified as a target gene of miR-449a. Both the high expression of miR-449a and low expression of MET reversed the inhibiting effects of LINC01106 knockdown on Ishikawa cells. Conclusion: Silencing of LINC01106 inhibits the occurrence and development of EC via regulating the miR-449a/MET axis. This study provides a possible therapeutic strategy for EC.

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Section: Introductionmentioning

confidence: 99%

<p>Silencing of Long Non-Coding RNA LINC01106 Suppresses the Proliferation, Migration and Invasion of Endometrial Cancer Cells Through Regulating the miR-449a/MET Axis</p>

Gao¹,

Yu²,

Zhang³

et al. 2020

OTT

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“…These measures are effective for early-stage EC. However, advanced, poorly differentiated or special types of EC are difficult to be treated and may ultimately produce poor results [3,4]. Most EC patients experience tumor recurrence or metastasis [5].…”

Section: Introductionmentioning

confidence: 99%

Knocking down of LINC01220 inhibits proliferation and induces apoptosis of endometrial carcinoma through silencing MAPK11

Yong

Kong

et al. 2019

Bioscience Reports

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Background: Endometrial carcinoma (EC) still threatens the health of women. Thus, to explore how long intergenic non-protein coding RNA 01220 regulates the development of EC. Methods: Whole genome expression profile data of EC and paracancerous tissues in TCGA database were downloaded. LINC01220 expression in EC and paracancerous tissues of patients in our hospital were detected by qRT-PCR. Furthermore, the relationship between LINC01220 expression and clinicopathological features of EC patients was analyzed. After transfection with sh-LINC01220 and pcDNA-MAPK11 (mitogen-activated protein kinase) in EC cells, proliferative, colony formation abilities and apoptosis were determined by cell counting kit-8 (CCK-8), colony formation assay and flow cytometry, respectively. Western blot was conducted to determine the regulatory role of LINC01220 on MAPK11. Results: TCGA data showed that LINC01220 expression is markedly higher in EC tissues than that of paracancerous tissues, which was consistent without detection in EC patients of our hospital. LINC01220 expression was positively correlated to pathological grade and International Federation of Gynecology and Obstetrics (FIGO) stage of EC patients. After knockdown of LINC01220 in EC cells, proliferative and colony formation abilities decreased, whereas apoptotic rate increased. Cor function analysis revealed the positive correlation between LINC01220 and MAPK11 in EC. MAPK11 expression was regulated by LINC01220 in EC cells. Overexpression of MAPK11 can reverse the tumor suppressing effect of LINC01220 on EC. Conclusions: LINC01220 promotes EC development by stimulating proliferation and inhibiting apoptosis of EC cells through up-regulating MAPK11.

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“…Nevertheless, only a minority of EC patients are sensitive to these treatments. 3 Moreover, type II EC patients have a poor prognosis with 5-year survival rate <35%. 4 Thus, identification of novel therapeutic targets and further elucidation of the molecular mechanisms underlying the tumorigenesis and progression of EC may have a major impact on the health of women.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of CLDN6 inhibits cell proliferation and migration via PI3K/AKT/mTOR signaling pathway in endometrial carcinoma cell line HEC-1-B

Cao

2018

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BackgroudDysregulation of claudin-6 (CLDN6) expression in cancers has been widely documented. However, no study has reported a complete mechanistic understanding of CLDN6 regulation and function in endometrial carcinoma (EC) progression. In the current study, we aimed to assess the expression and biological functions of CLDN6 in EC.MethodsFirstly, the expression level of CLDN6 in EC was measured based on The Cancer Genome Atlas (TCGA) database. Then, qRT-PCR and western blotting were implemented to detect the expression levels of CLDN6 in 82 pairs of EC tissues and corresponding non-tumor tissues, as well as EC cell line HEC-1B. After knockdown of CLDN6, with the attempt to assess whether CLDN6 reduction had positive effects on the cell proliferation, clone formation, invasion and migration abilities of HLC-1Bs, cell counting kit-8 (CCK-8) assay (24, 48, 72 and 96 hours post-transfection), clone experiment, and invasion and migration assays were conducted. Through western blotting analysis, CLDN6-mediated phosphatidylinositol 3-kinase (PI3K) pathway was evaluated.ResultsBased on the data of TCGA database, clinical patients and cell line HEC-1B, CLDN6 was up-regulated in EC compared with normal. Univariate as well as multivariate COX analysis indicated that CLDN6 expression can act as an independent prognostic factor for overall survival of EC. Further, knockdown of CLDN6 significantly inhibited HEC-1B cell proliferation, suppressed the colony numbers of HEC-1-B cells, and restrained the invasive and migratory ability of HEC-1-B cells. Importantly, through western blot analysis, we found that inhibition of CLDN6 remarkably decreased p-AKT, p-PI3K, and mTOR expression level in EC HEC-1B cell line.ConclusionOur data underscore the significance of CLDN6 in EC progression, and CLDN6 is a new candidate oncogene in EC. Our findings propose that targeting CLDN6 might offer future clinical utility in EC.

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Chemotherapy for advanced, recurrent or metastatic endometrial carcinoma

Cited by 21 publications

References 76 publications

<p>Silencing of Long Non-Coding RNA LINC01106 Suppresses the Proliferation, Migration and Invasion of Endometrial Cancer Cells Through Regulating the miR-449a/MET Axis</p>

<p>Silencing of Long Non-Coding RNA LINC01106 Suppresses the Proliferation, Migration and Invasion of Endometrial Cancer Cells Through Regulating the miR-449a/MET Axis</p>

Knocking down of LINC01220 inhibits proliferation and induces apoptosis of endometrial carcinoma through silencing MAPK11

Knockdown of CLDN6 inhibits cell proliferation and migration via PI3K/AKT/mTOR signaling pathway in endometrial carcinoma cell line HEC-1-B

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