ArticleDigestive diseases and sciences2018
Negative Regulation of Kruppel-Like Factor 4 on microRNA-106a at Upstream Transcriptional Level and the Role in Gastric Cancer Metastasis.
Article in Digestive diseases and sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- SAMHD1, positively regulated by KLF4, suppresses the proliferation of gastric cancer cells through MAPK p38 signaling pathway.Cell cycle (Georgetown, Tex.) · 2022Article
- Recent Discoveries on the Involvement of Krüppel-Like Factor 4 in the Most Common Cancer Types.International journal of molecular sciences · 2020Review
- Exosomal miR-106a derived from gastric cancer promotes peritoneal metastasis via direct regulation of Smad7.Cell cycle (Georgetown, Tex.) · 2020Article
- Analysis of the promoter region of the human miR-32 gene in colorectal cancer.Oncology letters · 2019Article
- Knockdown of miR-106a suppresses migration and invasion and enhances radiosensitivity of hepatocellular carcinoma cells by upregulating FBXW7.International journal of clinical and experimental pathology · 2019Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicroRNAs are classes of endogenous noncoding RNAs that play a substantial role in tumor processes through regulating the targets at posttranscriptional level. However, little is known about the upstream transcription regulatory mechanism although it is a prerequisite for investigation of its aberrant expression and function.
aimsThis report evaluates miR-106a's direct transcriptional factor from upstream level to in depth elucidate their communication in gastric cancer development.
methodsGastric cancer tissues were collected to analyze the miR-106a expression using real-time PCR methods. The combination of Kruppel (or Krüppel)-like factor 4 (KLF4) to miR-106a promoter was testified through bioinformatics followed by construction of luciferase reporter plasmid and chromatin immunoprecipitation assay. Functional experiments and mouse models for evaluating cell growth and metastasis were conducted to observe the biological effect of KLF4 on miR-106a. The interplay between KLF4 and miR-106a was tested with Wnt activator and confirmed in clinical specimens.
resultsThe up-regulated miR-106a linked to gastric cancer metastasis and epithelial-mesenchymal transition. UCSC and JASPAR predicted the promoter sequence of miR-106a and its binding site with transcriptional factor KLF4. Construction of reporter gene further verified their direct combination at upstream level. Moreover, the inhibitory effect of KLF4 on the phenotype of gastric cancer cells could be restored by miR-106a. CHIR-induced experiment and clinical specimens confirmed the negative regulation of KLF4 on miR-106a.
conclusionsOur findings provide novel direct insights into molecular mechanisms for interaction of KLF4 and miR-106a at upstream level and new ways for clinical application of KLF4-miR-106a axis in advanced gastric cancer metastasis.
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