MiR-135b-5p promotes viability, proliferation, migration and invasion of gastric cancer cells by targeting Kr üppel-like factor 4 (KLF4).

Conclusions: The inhibitory effects of ectopic KLF4 could be attenuated by co-transfection of miR-135b-5p. Collective data suggested that miR-135b-5p has a tumor-promoting role in GC cells via downregulating KLF4. Hence, inhibition of miR-135b-5p could be valuable for treatment of gastric cancer. PMID: 32051721 [PubMed]
Source: Archives of Medical Science - Category: General Medicine Tags: Arch Med Sci Source Type: research

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Source: Chinese Journal of Lung Cancer - Category: Cancer & Oncology Source Type: research
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Source: Experimental Cell Research - Category: Cytology Authors: Tags: Exp Cell Res Source Type: research
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Source: Advances in Experimental Medicine and Biology - Category: Research Tags: Adv Exp Med Biol Source Type: research
CagA gene transduction increases KLF4 promoter methylation level, which leads to inactivation of KLF4. Helicobacter pylori infection leads to KLF4 inactivation in gastric cancer through a TET1 ‐mediated DNA methylation mechanism. AbstractKr üppel‐like factor 4 (KLF4) has a tumor suppressor role in the progression of gastric cancer (GC), and inhibition or loss of KLF4 expression was identified in GC. The aim of this study was to explore the new molecular mechanism of KLF4 inactivation in gastric cancer. Herein, we report thatHelicobacter pylori infection or Cag pathogenicity island protein A (CagA) gene transductio...
Source: Cancer Medicine - Category: Cancer & Oncology Authors: Tags: ORIGINAL RESEARCH Source Type: research
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