2022
DOI: 10.1016/j.yexcr.2022.113131
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CTCF-activated SNHG16 facilitates gastrointestinal stromal tumor by targeting miR-128-3p/CASC3 axis

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Cited by 2 publications
(2 citation statements)
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“…For example, silencing the expression of SNHG16 could attenuate the proliferation, activate the apoptosis, and inhibit the migratory, invasive and malignant phenotype in GC cell lines. In addition, the knockdown of SNHG16 could reduce tumor volume and weight in a nude mouse human-GC xenograft model ( 173 ).…”
Section: Discussionmentioning
confidence: 99%
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“…For example, silencing the expression of SNHG16 could attenuate the proliferation, activate the apoptosis, and inhibit the migratory, invasive and malignant phenotype in GC cell lines. In addition, the knockdown of SNHG16 could reduce tumor volume and weight in a nude mouse human-GC xenograft model ( 173 ).…”
Section: Discussionmentioning
confidence: 99%
“…In addition, it has been shown that SNHG16 can promote EMT by downregulating the WNT signaling pathway and inhibiting DKK3 expression, and can regulate β-catenin protein expression without participating in the β-catenin translocation between the cytoplasm and nucleus ( 172 ). In particular, SNHG16 activated by CCCTC binding factor (CTCF) can modulate gastrointestinal stromal tumor cell proliferation, migration, invasion and apoptosis through the miR-128-3p/CASC3 axis ( 173 ). In another study, SNHG16 was also demonstrated to be able to mediate the upregulation of JAK2 and STAT3 by sponging miR-135a to influence the proliferation, invasion and apoptosis of GC cells, with SNHG16 being regulated by phosphorylated-STAT3 directly or indirectly ( 174 ).…”
Section: Snhg16 and Human Digestive System Cancermentioning
confidence: 99%