Dataset Information

RP11?619L19.2 promotes colon cancer development by regulating the miR?1271?5p/CD164 axis.

ABSTRACT: Colon cancer (CC) is one of the leading causes of cancer?related mortality in China and western countries. Several studies have demonstrated that long non?coding RNAs (lncRNAs) play critical roles in cancer development. However, the function of lncRNA RP11?619L19.2 in colon cancer remains unclear. The aim of the present study was to investigate the expression pattern, function and underlying mechanism of action of RP11?619L19.2 in CC development and metastasis. RP11?619L19.2 was found to be highly expressed in CC tissues and cell lines, and it was associated with advanced TNM stage and lymph node metastasis. Furthermore, knockdown of RP11?619L19.2 inhibited CC cell proliferation, migration, invasion and epithelial?to?mesenchymal transition (EMT). It was also observed that RP11?619L19.2 was reciprocally repressed by miR?1271?5p. Of note, miR?1271?5p negatively regulated CD164 expression by directly targeting the 3'?untranslated region of CD164. Overexpression of CD164 reversed the antimetastatic activity of RP11?619L19.2 knockdown in CC cells. Mechanistically, it was demonstrated that lncRNA RP11?619L19.2 played an oncogenic role and promoted CC development and metastasis by regulating the miR?1271?5p/CD164 axis and EMT. In conclusion, the findings of the present study indicated that RP11?619L19.2 regulates CD164 expression and EMT by sponging miR?1271?5p, which may provide novel targets for lncRNA?directed diagnosis and therapy for patients with CC.

SUBMITTER: Zhang XW

PROVIDER: S-EPMC7610312 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature

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RP11‑619L19.2 promotes colon cancer development by regulating the miR‑1271‑5p/CD164 axis.

Zhang Xin-Wu XW Li Shun-Le SL Zhang Di D Sun Xiao-Li XL Zhai Hong-Jun HJ

Oncology reports 20201007 6

Colon cancer (CC) is one of the leading causes of cancer‑related mortality in China and western countries. Several studies have demonstrated that long non‑coding RNAs (lncRNAs) play critical roles in cancer development. However, the function of lncRNA RP11‑619L19.2 in colon cancer remains unclear. The aim of the present study was to investigate the expression pattern, function and underlying mechanism of action of RP11‑619L19.2 in CC development and metastasis. RP11‑619L19.2 was found to be high ...[more]

PMID: 33125110

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Project description:The aim of the present study was to explore the effects of LINC00649 on the proliferation, migration and invasion of bladder cancer (BC) and identify possible mechanisms. Through TCGA database analysis of LINC00649 expression in bladder cancer and the association of LINC00649 with the BC patient prognosis, RT‑qPCR was employed for detecting LINC00649 expression in 60 clinical tissue specimens and cell lines of bladder cancer. The lentivirus stable transfection or small interfering RNA was used to increase or decrease the LINC00649 expression level in T24 and UM‑UC‑3 cells. CCK8 and clone formation assay were utilized to observe the effects of LINC00649 on the proliferation and colony formation of BC cells. Transwell experiment was performed to detect the effects of LINC00649 on the migration and invasion of bladder cancer. Bioinformatics database was used to identify the possible downstream targets of LINC00649 while RT‑qPCR, western blot analysis and dual luciferase reporter gene experiments were carried out to verify the possible molecular mechanism. The TCGA database analysis revealed a significantly high expression of LINC00649 in bladder cancer and an association of LINC00649 expression with overall survival rate of BC patients. As shown by RT‑qPCR detection, LINC00649 expression was notably upregulated in BC tissues and BC cell lines. In addition, statistical analyses unveiled that highly expressed LINC00649 was clearly associated with poor overall survival of bladder cancer. Based on the in vitro cell experiment, upregulated LINC00649 considerately enhanced the proliferation, migration and invasion of BC cells, as opposed to those in T24 and UM‑UC‑3 cells by suppressing LINC00649. Mechanically, LINC00649 may promote the malignant progression of bladder cancer by regulating miR‑15a‑5p to promote the HMGA1 expression axis. Overall, LINC00649 upregulates HMGA1 expression by binding to miR‑15a‑5p to enhance the proliferation, migration and invasion of BC cells. Thus, LINC00649 is a potential biomarker and therapeutic target for bladder cancer.

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Dataset Information

RP11?619L19.2 promotes colon cancer development by regulating the miR?1271?5p/CD164 axis.

Publications

RP11‑619L19.2 promotes colon cancer development by regulating the miR‑1271‑5p/CD164 axis.

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