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LINC01127 promotes the development of ovarian tumors by regulating the cell cycle.

ABSTRACT: BACKGROUND:Ovarian cancer is characterized by the high mortality rate and poor prognosis. Nevertheless, the oncogenesis mechanisms of ovarian cancer remain unclear. In our study, we focused on the potential role of lncRNA LINC01127 in the pathogenesis of ovarian cancer and its underlying mechanism. METHODS:LINC01127, which may participate in the development of ovarian cancer, was screened out by bioinformatics analysis. GSEA was used to analyze the function of LINC01127. QRT-PCR was used to analyze the LINC01127 level in 72 cases of ovarian cancer tissues and 53 cases of normal ovarian tissues. LINC01127 level in ovarian cancer cell lines was also determined by qRT-PCR. Subsequently, the selected ovarian tumor cells were transfected with LINC01127 siRNA by Lipofectamine 2000, followed by cell cycle detection using flow cytometry. The regulatory effects of LINC01127 on tumor growth and cell cycle in nude mice were verified by tumor formation assay. The mechanism of LINC01127 involving in cell cycle regulation was further explored by Western Blot. RESULTS:LINC01127 expression in ovarian cancer tissues was significantly higher than that in normal ovary tissues. The expression level of LINC01127 was negatively correlated with the prognosis of patients with ovarian cancer. GSEA analysis showed that LINC01127 was mainly enriched in the regulation of cell cycle. After transfection with LINC01127 siRNA, the proliferative abilities of SKOV3 and HO8910 cells were inhibited and cell cycle was arrested at G1/G0 phase. Tumorigenicity assay in nude mice showed that low expression of LINC01127 inhibited the growth of ovarian tumors. Further study found that LINC01127 knockdown upregulated expression levels of Cyclin D, Cyclin E and CDK4, but dramatically upregulated expression levels of P16 and P21. Meanwhile, the AKT and ERK pathways were inhibited by LINC01127 knockdown. CONCLUSIONS:LINC01127 was up-regulated in ovarian cancer tissues. LINC01127 may be involved in the development of ovarian cancer by accelerating cell cycle progression through promoting the phosphorylation of ERK and AKT.

SUBMITTER: Jing L

PROVIDER: S-EPMC6357339 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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LINC01127 promotes the development of ovarian tumors by regulating the cell cycle.

Jing Li L Gong Mi M Lu Xiaoyuan X Jiang Yi Y Li Huijian H Cheng Wenjun W

American journal of translational research 20190115 1

<h4>Background</h4>Ovarian cancer is characterized by the high mortality rate and poor prognosis. Nevertheless, the oncogenesis mechanisms of ovarian cancer remain unclear. In our study, we focused on the potential role of lncRNA LINC01127 in the pathogenesis of ovarian cancer and its underlying mechanism.<h4>Methods</h4>LINC01127, which may participate in the development of ovarian cancer, was screened out by bioinformatics analysis. GSEA was used to analyze the function of LINC01127. QRT-PCR w ...[more]

PMID: 30787997

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Project description:BackgroundOvarian cancer is one of the important factors that seriously threaten women's health and its morbidity and mortality ranks eighth among female cancers in the world. It is critical to identify potential and promising biomarkers for prognostic evaluation and molecular therapy of OV. Ubiquitin-conjugating enzyme E2S (UBE2S), a potential oncogene, regulates the malignant progression of various tumors; however, its role in OV is still unclear.MethodsThe expression and prognostic significance of UBE2S at the pan-cancer level were investigated through high-throughput gene expression analysis and clinical prognostic data from TCGA, GEPIA, and GEO databases. 181 patients with OV were included in this study. Cell culture and cell transfection were performed on OV cell lines (SKOV3 and A2780) and a normal ovarian cell line (IOSE80). The expression level and prognostic significance of UBE2S in OV were verified by western blot, immunohistochemistry, and Kaplan-Meier survival analysis. Through cell transfection, CCK-8, Ki-67 immunofluorescence, wound healing, Transwell, clonogenic, and flow cytometry assays, the effect and detailed mechanism of UBE2S knockdown on the malignant biological behavior of OV cells were explored.ResultsUBE2S exhibited abnormally high expression at the pan-cancer level. The results of RT-qPCR and Western blotting indicated that UBE2S was significantly overexpressed in ovarian cancer cell lines compared with normal cell lines (P < 0.05). Kaplan-Meier survival analysis and Immunohistochemistry indicated that overexpression of UBE2S was related to poor prognosis of OV (HR > 1, P < 0.05). Results of in vitro experiments indicated that UBE2S gene knockdown might inhibit the proliferation, invasion, and prognosis of OV cells by inhibiting the PI3K/AKT/mTOR signaling pathway, thereby blocking the cell cycle and promoting apoptosis (P < 0.05).ConclusionUBE2S is a potential oncogene strongly associated with a poor prognosis of OV patients. Knockdown of UBE2S could block the cell cycle and promote apoptosis by inhibiting the PI3K/AKT/mTOR pathway and ultimately inhibit the proliferation, migration and prognosis of ovarian cancer, which suggested that UBE2S might be used for molecular therapy and prognostic evaluation of ovarian cancer.

Project description:ObjectiveTo analyze the expression of hydroxysteroid dehydrogenase like 2 (HSDL2) in rectal cancer tissues and the effect of changes in HSDL2 expression level on proliferation of rectal cancer cells.MethodsClinical data and tissue samples of 90 patients with rectal cancer admitted to our hospital from January 2020 to June 2022 were collected from the prospective clinical database and biological specimen database. The expression level of HSDL2 in rectal cancer and adjacent tissues was detected by immunohistochemistry, and based on the median level of HSDL2 expression, the patients were divided into high expression group (n=45) and low expression group (n=45) for analysis the correlation between HSDL2 expression level and the clinicopathological parameters. GO and KEGG enrichment analyses were performed to explore the role of HSDL2 in rectal cancer progression. The effects of changes in HSDL2 expression levels on rectal cancer cell proliferation, cell cycle and protein expressions were investigated in SW480 cells with lentivirus-mediated HSDL2 silencing or HSDL2 overexpression using CCK-8 assay, flow cytometry and Western blotting.ResultsThe expressions of HSDL2 and Ki67 were significantly higher in rectal cancer tissues than in the adjacent tissues (P < 0.05). Spearman correlation analysis showed that the expression of HSDL2 protein was positively correlated with Ki67, CEA and CA19-9 expressions (P < 0.01). The rectal cancer patients with high HSDL2 expressions had significantly higher likelihood of having CEA ≥5 μg/L, CA19-9 ≥37 kU/L, T3-4 stage, and N2-3 stage than those with a low HSDL2 expression (P < 0.05). GO and KEGG analysis showed that HSDL2 was mainly enriched in DNA replication and cell cycle. In SW480 cells, HSDL2 overexpression significantly promoted cell proliferation, increased cell percentage in S phase, and enhanced the expression levels of CDK6 and cyclinD1 (P < 0.05), and HSDL2 silencing produced the opposite effects (P < 0.05).ConclusionThe high expression of HSDL2 in rectal cancer participates in malignant progression of the tumor by promoting the proliferation and cell cycle progress of the cancer cells.

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LINC01127 promotes the development of ovarian tumors by regulating the cell cycle.

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LINC01127 promotes the development of ovarian tumors by regulating the cell cycle.

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