Long non-coding RNA CCAT2 promotes epithelial-mesenchymal transition involving Wnt/β-catenin pathway in epithelial ovarian carcinoma cells

Wang, Beidi; Liu, Meimei; Zhuang, Ran; Jiang, Jing; Gao, Jiayin; Wang, Hao; Chen, He; Zhang, Zongfeng; Kuang, Ye; Li, Peiling

doi:10.3892/ol.2017.7669

Cited by 18 publications

(24 citation statements)

References 31 publications

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“…These results confirm a previous investigation wherein CCAT2 was shown to regulate the migration and invasion of cholangiocarcinoma cells [19]. In another study lncRNA was reported to exert its effects via regulation of the wnt/β-catenin signaling pathway in epithelial ovarian cancer cells [20]. The results showed that CCAT2 suppression also inhibits the wnt/β-catenin pathway in OVACAR-3 cells.…”

Section: Discussionsupporting

confidence: 90%

Long non-coding RNA CCAT2 regulates proliferation, drug sensitivity and metastasis of ovarian cancer

Han

Pan

et al. 2019

Arch Med Sci

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Introduction: Reports suggest that lncRNAs have implications in the development of several diseases including cancer. It is therefore believed that lncRNAs may act as therapeutic targets for cancer treatment. The treatment of ovarian cancer is mainly obstructed by lack of biomarkers and efficient drug targets. Against this backdrop, this study was undertaken to reveal the role and therapeutic implications of lncRNA CCAT2 in ovarian cancer. Material and methods: Expression analysis was carried out with quantitative real-time polymerase chain reaction (qRT-PCR). Transfections were carried out using Lipofectamine 2000 reagent. Cell counting kit 8 (CCK-8) assays were used to determine the cell viability. AO/EB and annexin V/ propidium iodide (PI) were used for detection of apoptosis. Wound healing and transwell assays were used to determine cell migration and invasion. The expression of the proteins was estimated by western blotting. Results: The results showed that the expression of CCAT2 was significantly overexpressed in ovarian cancer tissues and cell lines. Si-RNA mediated silencing of CCAT2 resulted in the decrease of proliferation rate and colony formation potential of the OVACAR-3 cells via induction of apoptotic cell death, which was also accompanied by cleavage of PARP, downregulation of Bcl-2 and upregulation of Bax, caspase-3 and caspase-9. Suppression of CCAT2 enhanced the chemosensitivity of the OVACAR-3 cells to cisplatin and also decreased their migration and invasion. Conclusions: The findings of this study revealed that lncRNA CCAT2 suppression inhibits the proliferation, drug sensitivity, and metastasis of ovarian cancer and may prove beneficial in ovarian cancer management.

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Section: Discussionsupporting

confidence: 90%

Long non-coding RNA CCAT2 regulates proliferation, drug sensitivity and metastasis of ovarian cancer

Han

Pan

et al. 2019

Arch Med Sci

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“…[30][31][32] We suspected that the autophagy may be activated in GC cells to protect against apoptosis. The action mechanisms of CCAT2 on tumors are complex, which involve diverse regulatory factors, such as E-cadherin/LATS2, 10 P15, 33 GSK3β/β-catenin, 34 Wnt/ β-catenin, 35 and TGF-β. 21 In this study, the specific regulatory relationship between CCAT2 and mTOR signaling was evaluated.…”

Section: Discussionmentioning

confidence: 99%

<p>Silencing of Long Non-Coding RNA Colon Cancer-Associated Transcript 2 Inhibits the Growth and Metastasis of Gastric Cancer Through Blocking mTOR Signaling</p>

Shi¹,

Wang²,

Yang³

et al. 2020

OTT

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Purpose: This study aimed to evaluate the specific role of colon cancer-associated transcript 2 (CCAT2) on gastric cancer (GC), and reveal the potential regulatory mechanism relating to mammalian target of rapamycin (mTOR) signaling. Methods: The expression of CCAT2 was detected in GC tissues and cells by quantitative real-time PCR (qRT-PCR), and its relation with the pathologic characteristics of GC patients was analyzed. HGC-27 and SGC-7901 cells were transfected with siRNA-CCAT2 to silence CCAT2, and HGC-27 cells were then treated with an mTOR agonist Leucine (Leu) to activate mTOR signaling. The cell proliferation was evaluated by cell viability and colony formation. The cell cycle and apoptosis, and the migration and invasion abilities were detected by Flow cytometry, and Transwell assay, respectively. The expression of PCNA (proliferation marker), Snail, N-cadherin, E-cadherin (invasion markers), P53, Caspase-8, Bcl-2 (apoptosis markers), LC3-II/LC3-I, ATG3, p62 (autophagy makers), phosphorylated mTOR (p-mTOR), p-AKT, and p-p70S6K (mTOR signaling markers) were detected by Western blot. Results: CCAT2 was upregulated in GC tissues and cells, and positively associated with the maximum tumor diameter, lymphatic metastasis, TNM staging, and low overall survival rate (P < 0.05). siRNA-CCAT2 transfection significantly inhibited the viability, colony formation, and migration and invasion abilities, blocked the cell cycle in G0/G1 phase, and promoted the apoptosis and autophagy of SGC-7901 and HGC-27 cells (P < 0.05). In addition, siRNA-CCAT2 transfection significantly upregulated P53, Caspase-8, LC3-II/LC3-I and ATG3, and downregulated PCNA, Bcl-2, p62, p-mTOR, p-AKT and p-p70S6K in SGC-7901 and HGC-27 cells (P < 0.05). siRNA-CCAT2 reversed the tumor-promoting effect of mTOR signaling activation on HGC-27 cells (P < 0.05). Conclusion: Silencing of CCAT2 inhibited the proliferation, migration and invasion, and promoted the apoptosis and autophagy of GC cells through blocking mTOR signaling.

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“…As a matter of fact, CCAT2 has been certified as an oncogene in other neoplasms. [31][32][33] In particular, suppression of in-vitro CCAT2 expression was able to hinder both proliferation and invasion of breast cancer cells, and tumor growth in animal models was also restrained by lowly expressed CCAT2. 34 Moreover, dysfunctional CCAT2, due to mutation of alleles in rs6983267, also boosted aggravation of colorectal cancer through affecting Wnt signaling, 35 but whether SNP rs6983267 also played an analogous part underlying glioma pathogenesis was unknown.…”

Section: Discussionmentioning

confidence: 99%

<p>lncRNA CCAT2 Enhanced Resistance of Glioma Cells Against Chemodrugs by Disturbing the Normal Function of miR-424</p>

Ding¹,

Zhang²,

Chen³

et al. 2020

OTT

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These authors contributed equally to this workBackground: Aggressive metastasis of tumor cells assumed a constructive role in strengthening chemoresistance of tumors, so this investigation was intended to elucidate if lncRNA CCAT2 sponging downstream miR-424 regulated chemotolerance of glioma cells by boosting metastasis of glioma cells. Methods: One hundred and twenty-eight pairs of glioma tissues and corresponding adjacent tissues were resected from glioma patients during their operation, and we also purchased a series of glioma cell lines, including U251, U87, A172 and SHG44. Furthermore, pcDNA3.1-CCAT2, si-CCAT2, miR-424 mimic and miR-424 inhibitor were transfected into SHG44 and U251 cell lines, so as to evaluate impacts of CCAT2 and miR-424 on chemosensitivity of the glioma cells. Besides, proliferation, invasion and metastasis of the cells were determined through the implementation of colony formation assay, transwell assay and scratch assay. Results: Glioma tissues and cells were monitored with higher CCAT2 expression and lower miR-424 expression than adjacent normal tissues and NHA cell line (P<0.05). Among the glioma cell lines, the SHG44 cell line showed the strongest resistance against teniposide, temozolomide and cisplatin (P<0.05), whereas the U251 cell line was more sensitive to teniposide, temozolomide, vincristine and cisplatin than any other cell line (P<0.05). Besides, pcDNA3.1-CCAT2 and miR-424 inhibitor could enhance tolerance of glioma cell lines against drugs (P<0.05). Moreover, in-vitro transfection of si-CCAT2 and miR-424 mimic could significantly retard proliferation, invasion and migration of SHG44 and U251 cells (P<0.05), and CCAT2 was found to negatively regulate miR-424 expression by sponging it (P<0.05). In addition, CHK1 was deemed as the molecule targeted by upstream miR-424, and its overexpression can changeover the effects of miR-424 mimic on proliferation and metastasis of SHG44 and U251 cells. Conclusion: lncRNA CCAT2/miR-424/Chk1 axis might serve as a promising target for improving chemotherapeutic efficacies in glioma treatment.

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Long non-coding RNA CCAT2 promotes epithelial-mesenchymal transition involving Wnt/β-catenin pathway in epithelial ovarian carcinoma cells

Cited by 18 publications

References 31 publications

Long non-coding RNA CCAT2 regulates proliferation, drug sensitivity and metastasis of ovarian cancer

Long non-coding RNA CCAT2 regulates proliferation, drug sensitivity and metastasis of ovarian cancer

<p>Silencing of Long Non-Coding RNA Colon Cancer-Associated Transcript 2 Inhibits the Growth and Metastasis of Gastric Cancer Through Blocking mTOR Signaling</p>

<p>lncRNA CCAT2 Enhanced Resistance of Glioma Cells Against Chemodrugs by Disturbing the Normal Function of miR-424</p>

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