scholarly journals LINC02418 promotes colon cancer progression by suppressing apoptosis via interaction with miR-34b-5p/BCL2 axis

2020 ◽  
Author(s):  
Jun Tian ◽  
Peng Cui ◽  
Yifei Li ◽  
Xuequan Yao ◽  
Xiaoyu Wu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Human Colon ◽  
Luciferase Assay ◽  
Colon Cancer Cells ◽  
Multiple Cancer ◽  
Human Colon Cancer ◽  
Prediction Of Prognosis

Abstract Background LncRNAs have been demonstrated to be functional regulators in tumor progression through interaction with various signaling pathways in multiple cancer types. However, the effect of LINC02418 on CRC progression still remains unclear. Methods LncRNA expression profile in CRC tissues was explored by using the TCGA database. The expressional level of LINC02418 in CRC patients was confirmed by qRT-PCR. Kaplan-Meier analyses was used to investigate the correlations between LINC02418 and OS of patients with CRC. After stably transducing sh-LINC02418 and sh-NC into HCT116 and LoVo cells, cell proliferative, migratory and invasive abilities were detected by CCK-8 assay, colony formation assay and trans-well assay, respectively. The binding between LINC02418 and miR-34b-5p, and the interaction between miR-34b-5p and BCL2 were determined by dual-luciferase assay. Western blot experiments were conducted to further explore the effect of miR-34b-5p on BCL2 signaling pathway. Rescue experiments were performed to uncover the role of LINC02418 /miR-34b-5p/ BCL2 axis in CRC progression. Results LINC02418 was upregulated in human colon cancer samples and its high expression correlated with poor prognosis. LINC02418 promoted cancer progression by enhancing tumor growth, cell mobility and invasiveness of colon cancer cells. Additionally, LINC02418 could physically bind to miR-34b-5p and subsequently interact with BCL2 signaling pathway. Down-regulation of LINC02418 reduced cell proliferation, but transfection of miR-34b-5p inhibitor or BCL2 in LINC02418-silenced colon cancer cells significantly promoted cell growth. Conclusions LINC02418 was upregulated in human colon cancer samples and could be used as indicator for prediction of prognosis. LINC02418 acted as a tumor driver by negatively regulating cell apoptosis through LINC02418 /miR-34b-5p/ BCL2 axis and in colorectal cancer.

scholarly journals LINC02418 promotes colon cancer progression by suppressing apoptosis via interaction with miR-34b-5p/BCL2 axis

2020 ◽  
Author(s):  
Jun Tian ◽  
Peng Cui ◽  
Yifei Li ◽  
Xuequan Yao ◽  
Xiaoyu Wu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Human Colon ◽  
Luciferase Assay ◽  
Colon Cancer Cells ◽  
Multiple Cancer ◽  
Human Colon Cancer ◽  
Prediction Of Prognosis

Abstract Background LncRNAs have been demonstrated to be functional regulators in tumor progression through interaction with various signaling pathways in multiple cancer types. However, the effect of LINC02418 on CRC progression still remains unclear. Methods LncRNA expression profile in CRC tissues was explored by using the TCGA database. The expressional level of LINC02418 in CRC patients was confirmed by qRT-PCR. Kaplan-Meier analyses was used to investigate the correlations between LINC02418 and OS of patients with CRC. After stably transducing sh-LINC02418 and sh-NC into HCT116 and LoVo cells, cell proliferative, migratory and invasive abilities were detected by CCK-8 assay, colony formation assay and trans-well assay, respectively. The binding between LINC02418 and miR-34b-5p, and the interaction between miR-34b-5p and BCL2 were determined by dual-luciferase assay. Western blot experiments were conducted to further explore the effect of miR-34b-5p on BCL2 signaling pathway. Rescue experiments were performed to uncover the role of LINC02418 /miR-34b-5p/ BCL2 axis in CRC progression. Results LINC02418 was upregulated in human colon cancer samples and its high expression correlated with poor prognosis. LINC02418 promoted cancer progression by enhancing tumor growth, cell mobility and invasiveness of colon cancer cells. Additionally, LINC02418 could physically bind to miR-34b-5p and subsequently interact with BCL2 signaling pathway. Down-regulation of LINC02418 reduced cell proliferation, but transfection of miR-34b-5p inhibitor or BCL2 in LINC02418-silenced colon cancer cells significantly promoted cell growth. Conclusions LINC02418 was upregulated in human colon cancer samples and could be used as indicator for prediction of prognosis. LINC02418 acted as a tumor driver by negatively regulating cell apoptosis through LINC02418 /miR-34b-5p/ BCL2 axis and in colorectal cancer.

scholarly journals Correlation of GOLPH3 Gene with Wnt Signaling Pathway in Human Colon Cancer Cells

2016 ◽  
Vol 7 (8) ◽  
pp. 928-934 ◽  
Author(s):  
Cheng-Zhi Qiu ◽  
Ming-Zhen Wang ◽  
Wai-Shi Yu ◽  
Yan-Ta Guo ◽  
Chun-Xiao Wang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Wnt Signaling ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Wnt Signaling Pathway ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells

scholarly journals HRT, Herbal Formula, Induces G2/M Cell Cycle Arrest and Apoptosis via Suppressing Akt Signaling Pathway in Human Colon Cancer Cells

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Nam-Hui Yim ◽  
Won-Kyung Cho ◽  
Ju Hye Lee ◽  
Young Pil Jung ◽  
Hye Jin Yang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
M Cell ◽  
Human Colon Cancer ◽  
Cycle Arrest

We have demonstrated the anticancer effect of HRT in HCT116, human colon carcinoma cells. HRT inhibited cancer cell growth by causing cell cycle arrest at G2/M and inducing apoptosis as evidenced by DNA fragmentation assay. We found that HRT induces the activation of caspase-3, -8, and -9, whereas it reduces the level of Bcl-2 protein and results in the cleavage of PARP. Further, HRT decreased the level of phosphorylation of Akt and its downstream signals such as mTOR and GSK-3β. These results indicate that HRT stimulates the apoptotic signaling pathway and represses the survival and proliferation of colon cancer cells via inhibiting Akt activity. Hence, our results suggest that HRT has a potential to be developed as a therapeutic agent against colon cancer cells.

scholarly journals LINC02418 promotes colon cancer progression by suppressing apoptosis via interaction with miR-34b-5p/BCL2 axis

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Jun Tian ◽  
Peng Cui ◽  
Yifei Li ◽  
Xuequan Yao ◽  
Xiaoyu Wu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Human Colon ◽  
Human Colon Cancer ◽  
Kaplan Meier ◽  
Lovo Cells ◽  
Colon Cancer Progression ◽  
Prediction Of Prognosis

Abstract Background LncRNAs act as functional regulators in tumor progression through interacting with various signaling pathways in multiple types of cancer. However, the effect of LINC02418 on colorectal cancer (CRC) progression and the underling mechanisms remain unclear. Methods LncRNA expression profile in CRC tissues was investigated by the TCGA database. The expressional level of LINC02418 in CRC patients was determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Kaplan–Meier analyses was used to investigate the correlation between LINC02418 and overall survival (OS) of CRC patients. Cell proliferative, migratory and invasive abilities were detected by CCK-8 assays, colony formation assays and trans-well assays in HCT116 and LoVo cells which were stably transduced with sh-LINC02418 or sh-NC. The binding between LINC02418 and miR-34b-5p, and the interaction between miR-34b-5p and BCL2 were determined by dual-luciferase assays. Western blot experiments were conducted to further explore the effect of miR-34b-5p on BCL2 signaling pathway. Rescue experiments were performed to uncover the role of LINC02418/miR-34b-5p/BCL2 axis in CRC progression. Results LINC02418 was upregulated in human colon cancer samples when compared with adjacent tissue, and its high expressional level correlated with poor prognosis of CRC patients. LINC02418 promoted cancer progression by enhancing tumor growth, cell mobility and invasiveness of colon cancer cells. Additionally, LINC02418 could physically bind to miR-34b-5p and subsequently affect BCL2 signaling pathway. Down-regulation of LINC02418 reduced cell proliferation, while transfection of miR-34b-5p inhibitor or BCL2 into LINC02418-silenced CRC cells significantly promoted CRC cells growth. Conclusions LINC02418 was upregulated in human CRC samples and could be used as the indicator for prediction of prognosis. LINC02418 acted as a tumor driver by negatively regulating cell apoptosis through LINC02418/miR-34b-5p/BCL2 axis in CRC.

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