Arab journal of gastroenterology : the official publication of the Pan-Arab Association of Gastroenterology · 2023
AC125611.3 promotes the progression of colon cancer by recruiting DKC1 to stabilize CTNNB1.
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Tang Hanqing, Dou Yuyu, Meng Yiliang, Lu Qinglan, Liang Lingling
Аннотация
BACKGROUND AND STUDY AIMS: Previous studies have suggested that lncRNAs impact cancer progression. The lncRNA AC125611.3 (also referred to as RP11-161H23.5) is highly expressed in colon cancer but rarely studied; understanding its regulation may provide novel insights on treating colon cancer.
MATERIALS AND METHODS: qRT-PCR was performed to quantify RNAs. CCK-8 and EdU assays were performed to assess cell proliferation. Western blot analysis was used to detect levels of proteins related to cell apoptosis and EMT. Wound healing assay and Transwell invasion assay were conducted to evaluate cell migratory and invasive capabilities, respectively. Luciferase reporter assay, RIP assay, and pull-down assay were used to verify RNA-RNA and RNA-protein interactions.
RESULTS: AC125611.3 was highly overexpressed in colon cancer cells. AC125611.3 depletion curbed cell proliferative, invasive, migratory, and EMT processes while enhancing apoptosis. Furthermore, AC125611.3 activated the Wnt signaling pathway in colon cancer cells by regulating catenin beta-1 (CTNNB1). Moreover, AC125611.3 recruited dyskeratosis congenita 1 (DKC1) to stabilize CTNNB1.
CONCLUSION: AC125611.3 recruits DKC1 to stabilize CTNNB1 and activate Wnt signaling, thereby promoting the progression of colon cancer.
MATERIALS AND METHODS: qRT-PCR was performed to quantify RNAs. CCK-8 and EdU assays were performed to assess cell proliferation. Western blot analysis was used to detect levels of proteins related to cell apoptosis and EMT. Wound healing assay and Transwell invasion assay were conducted to evaluate cell migratory and invasive capabilities, respectively. Luciferase reporter assay, RIP assay, and pull-down assay were used to verify RNA-RNA and RNA-protein interactions.
RESULTS: AC125611.3 was highly overexpressed in colon cancer cells. AC125611.3 depletion curbed cell proliferative, invasive, migratory, and EMT processes while enhancing apoptosis. Furthermore, AC125611.3 activated the Wnt signaling pathway in colon cancer cells by regulating catenin beta-1 (CTNNB1). Moreover, AC125611.3 recruited dyskeratosis congenita 1 (DKC1) to stabilize CTNNB1.
CONCLUSION: AC125611.3 recruits DKC1 to stabilize CTNNB1 and activate Wnt signaling, thereby promoting the progression of colon cancer.