Su1734 Canonical Wnt Signals Combined With Suppressed TGFbeta/BMP Pathways Promote Renewal of the Native Human Colonic Epithelium

Wharton, Natalia; Parris, Alyson; Reynolds, Amy; Mitchell, Esther M.; Sobolewski, Anastasia; Hadi, Ahmed El; Lewis, Michael P.; Speakman, Chris; Stebbings, William; Wharton, Richard; Sargen, Kevin; Tighe, R; Jamieson, Crawford P.; Hernon, James; Kapur, Sandeep; Williams, Mark Richard James

doi:10.1016/s0016-5085(13)61712-6

“…The progress of normal intestinal epithelial cell transition to unregulated cancer cell is a multi-stage and complicated process which is associated with the accumulation of both genetic and epigenetic changes. The aberration, mutations of oncogenes or tumor suppressive genes, and epigenetic alterations all lead to the progression of CRC [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

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

Tian

¹

,

Cui

²

,

Li

³

et al. 2020

Preprint

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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.

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“…The progress of normal intestinal epithelial to CRC is a multi-stage and complicated process which is associated with the accumulation of both genetic and epigenetic changes. The aberration, mutations of several suppressive genes or oncogenes, and epigenetic alteration contribute to the progression of CRCs [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

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

Tian

¹

,

Cui

²

,

Li

³

et al. 2020

Preprint

0

View full text Add to dashboard Cite

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.

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Anti-ulcerative colitis effect of rotating magnetic field on DSS-induced mice by modulating colonic inflammatory deterioration

Yang,

Zhou,

Nie

et al. 2024

Molecular Immunology

0

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Su1734 Canonical Wnt Signals Combined With Suppressed TGFbeta/BMP Pathways Promote Renewal of the Native Human Colonic Epithelium

Cited by 3 publications

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

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

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

Anti-ulcerative colitis effect of rotating magnetic field on DSS-induced mice by modulating colonic inflammatory deterioration

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