LncRNA HOXD-AS1 promotes epithelial ovarian cancer cells proliferation and invasion by targeting miR-133a-3p and activating Wnt/β-catenin signaling pathway

Zhang, Ying; Dun, Yanbing; Zhou, Shumin; Huang, Xianghua

doi:10.1016/j.biopha.2017.11.096

Cited by 75 publications

(65 citation statements)

References 23 publications

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“…Abnormal expression of TIMP2 has been implicated in growth and invasion of multiple malignant tumors . Several upstream factors have been reported to mediate tumor progression and metastasis through the TIMP2 . For instance, EZH2 was found to promote metastasis via TIMP2 signaling pathway in EOC .…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: lncRNA ABHD11‐AS1, regulated by the EGFR pathway, contributes to the ovarian cancer tumorigenesis by epigenetically suppressing TIMP2

et al. 2019

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ObjectiveEpithelial ovarian cancer (EOC) is a common gynecologic malignancy characterized by extensive peritoneal metastasis and high mortality rate. ABHD11 Antisense RNA1 (ABHD11‐AS1) has recently been identified as a regulator of growth and metastasis in multiple tumors, including EOC. However, the biological function and potential mechanism of ABHD11‐AS1 in EOC remains poorly understood.MethodsImmunohistochemistry, western blot, and qRT‐PCR analysis were used to determine the expression pattern of ABHD11‐AS1 and epidermal growth factor receptor (EGFR) in both EOC tissues and cell lines, respectively. Colony formation, transwell and wound healing assays were performed to evaluate the roles of EGFR and ABHD11‐AS1 on the capacity of cell proliferation, migration, and invasion. Western blot analysis was performed to measure the regulation of EGFR pathway on STAT3. Moreover, chromatin immunoprecipitation was employed to demonstrate the interaction between ABHD11‐AS1 and STAT3. RNA immunoprecipitation was subjected to prove the direct binding between ABHD11‐AS1 and EZH2. Immunofluorescence staining was performed to measure the expression and localization of TIMP2. EOC mouse model was conducted for validating the role of ABHD11‐AS1 in vivo.ResultsEGFR and ABHD11‐AS1 were highly expressed in EOC tissues and cell lines. Knockdown of EGFR or ABHD11‐AS1 inhibited cell growth, migration, and invasion of EOC cells. Expression of ABHD11‐AS1 was regulated by the activation of EGFR signaling pathway, mediated by STAT3. Besides, ABHD11‐AS1 was shown to silence TIMP2 by binding to chromatin‐modifying enzyme EZH2. Furthermore, inhibition of EGFR pathway or ABHD11‐AS1 repressed the tumor growth of EOC.ConclusionWe defined the regulatory relationship between the EGFR signaling pathway, ABHD11‐AS1, EZH2, and TIMP2 suggesting that ABHD11‐AS1 may act as an oncogene and a potential target for antitumor therapies in ovarian cancer.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: lncRNA ABHD11‐AS1, regulated by the EGFR pathway, contributes to the ovarian cancer tumorigenesis by epigenetically suppressing TIMP2

et al. 2019

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“…7 Metastasis-associated lung adenocarcinoma transcript-1 (MALAT1) was proved to be an oncogenic lncRNA and promoted proliferation and invasion in ovarian cancer cells. [9][10][11] However, the exact contributions of lncRNAs to ovarian cancer remain largely unknown. [9][10][11] However, the exact contributions of lncRNAs to ovarian cancer remain largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA DQ786243 interacts with miR‐506 and promotes progression of ovarian cancer through targeting cAMP responsive element binding protein 1

Yan

Silva

et al. 2018

J of Cellular Biochemistry

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Long noncoding RNAs (lncRNAs) have been reported to be abnormally expressed in several cancers and associated with the proliferation of cancer cells. The objective of this study was to investigate the role and the underlying mechanisms of DQ786243 in ovarian cancer. In the current study, DQ786243 was specifically upregulated in ovarian cancer tissues and cell lines. Knockdown of DQ786243 inhibited the ability of cell migration, invasion, proliferation, colony formation and wound healing, whereas promoted cell apoptosis and induced G0/G1 cell cycle arresting. By using online tools and mechanistic analysis, we demonstrated that DQ786243 could directly bind to microRNA-506 (miR-506) and downregulate its expression. Moreover, DQ786243 reversed the inhibitory effect of miR-506 on the growth of ovarian cancer cells, which might be involved in the derepression of cAMP responsive element binding protein 1 (CREB1) expression. Further investigation into the mechanisms showed that knockdown of DQ786243 inhibited the epithelial to mesenchymal transition (EMT) process in ovarian cancer cells. Finally, xenograft experiments further confirmed that knockdown of DQ786243 notably suppressed the proliferation and EMT process in vivo. Taken together, our study showed for the first time that DQ786243 interacted with miR-506 and promoted progression of ovarian cancer via targeting CREB1 in ovarian cancer. The results might help to probe the feasibility of lncRNA-directed therapy for this deadly disease.

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“…LncRNA LINC00968 can promote non–small‐cell lung carcinoma progression and tumorigenesis via activating the Wnt signaling pathway . LncRNA HOXD‐AS1 can promote epithelial ovarian cancer cells proliferation and invasion through targeting miR‐133a‐3p and activating Wnt/β‐catenin pathway . LncRNA HNF1A‐AS1 can indicate a poor prognosis of colorectal cancer via activation of Wnt/β‐catenin .…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA DGCR5 represses hepatocellular carcinoma progression by inactivating Wnt signaling pathway

Wang

Shi

Xiang

et al. 2018

J of Cellular Biochemistry

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Increasing studies have indicated that long noncoding RNAs (lncRNAs) exert important roles in hepatocellular carcinoma (HCC). Therefore, it is of great significance to identify the dysregulated lncRNAs in HCC. According to the previous reports, it has been suggested that DiGeorge syndrome critical region gene 5 (DGCR5) might participate in HCC and can serve as potential biomarker for HCC. In our current study, we concentrated on the biological function and roles of lncRNA‐DGCR5 in HCC. It was indicated that DGCR5 was decreased in HCC tissues and HCC cells including HepG2, Hep3B, MHCC‐97L, SNU‐449, and SNU‐182 cells compared with the normal human liver cell line LO2. Overexpression of DGCR5 was able to restrain HCC growth, migration, and invasion capacity in HepG2 and SNU‐449 cells. In addition, whether lncRNA‐DGCR5 can regulate Wnt/β‐catenin pathway during HCC progression is unclear. In our study, it was found that upregulation of DGCR5 inactivated Wnt signaling pathway through inhibiting β‐catenin, cyclin D1 and increasing GSK‐3β levels. Subsequently, in vivo tumor xenografts were established using HepG2 cells to investigate the function of DGCR5 in HCC development. Inconsistent with the in vitro findings, increase of DGCR5 dramatically suppressed HCC tumor progression in vivo. Taken these together, it was uncovered in our research that DGCR5 could play tumor suppressive role by targeting Wnt signaling in HCC progression.

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LncRNA HOXD-AS1 promotes epithelial ovarian cancer cells proliferation and invasion by targeting miR-133a-3p and activating Wnt/β-catenin signaling pathway

Cited by 75 publications

References 23 publications

RETRACTED: lncRNA ABHD11‐AS1, regulated by the EGFR pathway, contributes to the ovarian cancer tumorigenesis by epigenetically suppressing TIMP2

RETRACTED: lncRNA ABHD11‐AS1, regulated by the EGFR pathway, contributes to the ovarian cancer tumorigenesis by epigenetically suppressing TIMP2

Long noncoding RNA DQ786243 interacts with miR‐506 and promotes progression of ovarian cancer through targeting cAMP responsive element binding protein 1

Long noncoding RNA DGCR5 represses hepatocellular carcinoma progression by inactivating Wnt signaling pathway

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