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CRKL overexpression promotes cell proliferation and inhibits apoptosis in endometrial carcinoma.

ABSTRACT: The v-Crk avian sarcoma virus CT10 oncogene homolog-like (CRKL) protein is important in cancer progression. However, its expression pattern and biological roles in human endometrial carcinoma remain unexplored. The potential mechanism of CRKL-induced cancer progression is still unclear. The present study aimed to explore the expression pattern and biological roles of CRKL in human endometrial carcinoma. Using immunohistochemistry, it was observed that the CRKL protein was overexpressed in 50.5% (44/87) of endometrial carcinoma tissues. Plasmid transfection of CRKL into Ishikawa cells was performed, and CRKL overexpression promoted cell proliferation, colony formation and cell cycle transition in the transfected cells. In addition, CRKL overexpression inhibited cell apoptosis in Ishikawa cells treated with cisplatin, with decreased caspase-3 and caspase-9 cleavage. Further analysis revealed that CRKL upregulated the expression of cyclin D1, cyclin E, B cell lymphoma (Bcl)-2 and survivin, and downregulated Bcl-2 associated X protein expression. In conclusion, the present study demonstrated that CRKL overexpression in endometrial carcinoma contributes to malignant cell growth and resistance to apoptosis, possibly through Bcl-2.

SUBMITTER: Cai L

PROVIDER: S-EPMC5245097 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature

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CRKL overexpression promotes cell proliferation and inhibits apoptosis in endometrial carcinoma.

Cai Le L Wang He H Yang Qing Q

Oncology letters 20161117 1

The v-Crk avian sarcoma virus CT10 oncogene homolog-like (CRKL) protein is important in cancer progression. However, its expression pattern and biological roles in human endometrial carcinoma remain unexplored. The potential mechanism of CRKL-induced cancer progression is still unclear. The present study aimed to explore the expression pattern and biological roles of CRKL in human endometrial carcinoma. Using immunohistochemistry, it was observed that the CRKL protein was overexpressed in 50.5% ...[more]

PMID: 28123521

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Project description:Endometrial carcinoma (EC) is the most common cancer in women worldwide, yet little is known about the underlying molecular basis of EC development. LINC01224, a novel long non‑coding (lnc)RNA, was recently identified as an oncogene in various types of cancer. However, the function and underlying mechanism of LINC01224 in EC is still unclear. A total of 50 pairs of tumor and adjacent normal tissue from patients with EC, three EC cell lines and one human normal endometrial stromal cell (ESC) line were subjected to reverse transcription‑quantitative PCR assay to evaluate the expression levels of LINC01224. Cell Counting Kit‑8, colony formation and flow cytometry assays were used to assess cell proliferation and apoptosis. Western blotting was used to measure expression levels of apoptosis‑ and proliferation‑associated proteins and AKT3 protein. A xenograft model of HEC1A cells was established to validate the in vivo function of LINC01224 in EC tumor growth. Starbase 3.0 database prediction and luciferase reporter and RNA pull‑down assays were performed to verify the binding sites between LINC01224 and microRNA (miR)‑485‑5p and miR‑485‑5p and AKT3. LINC01224 expression was significantly upregulated in both EC tumor tissue and cell lines. The upregulation of LINC01224 was negatively associated with survival of patients with EC. Functionally, LINC01224 promoted proliferation and inhibited apoptosis of EC cells; LINC01224 directly bound to and downregulated miR‑485‑5p to elevate the expression levels of AKT3, thereby promoting EC progression. LINC01224 depletion in EC cells hindered tumor growth in a xenograft model. The tumor suppressing effect of LINC01224‑knockdown on EC progression was partly rescued by treatment with miR‑485‑5p inhibitor. The present data demonstrated the expression levels, clinical relevance and functional mechanism of LINC01224 in EC. LINC01224 promoted EC development via sponging miR‑485‑5p to elevate AKT3 expression levels; this may provide a promising therapeutic target pathway for EC treatment.

Dataset Information

CRKL overexpression promotes cell proliferation and inhibits apoptosis in endometrial carcinoma.

Publications

CRKL overexpression promotes cell proliferation and inhibits apoptosis in endometrial carcinoma.

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