ArticleAmerican journal of translational research2022
Shortening of the KHDRBS1 3'UTR by alternative cleavage and polyadenylation alters miRNA-mediated regulation and promotes gastric cancer progression.
Article in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- CSTF2-mediated 3'UTR shortening drives oncogenic activation of GPC3 in hepatocellular carcinoma.Oncogene · 2026Article
- Abnormal levels of miRNA in pancreatic cancer are linked to tumor progression by regulating the translation of tumor-associated mRNA.Annals of medicine · 2025Review
- Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025Review
- KHDRBS1 regulates the pentose phosphate pathway and malignancy of GBM through SNORD51-mediated polyadenylation of ZBED6 pre-mRNA.Cell death & disease · 2024Article
- Bioinformatics Analysis of Biomarkers and Therapeutic Targets Related to Necroptosis in Intervertebral Disc Degeneration.BioMed research international · 2024Article
- Interplay of four types of RNA modification writers revealed distinct tumor microenvironment and biological characteristics in pancreatic cancer.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The shortening of the 3' untranslated regions (3'UTRs) due to alternative polyadenylation (APA) has become an important characteristic of cancer. However, the function of APA-induced 3'UTR shortening in gastric cancer (GC) remains unclear. KHDRBS1 (sam68), as an RNA-binding protein (RBP), is significantly upregulated in GC. In this study, we found that the 3'UTR of KHDRBS1 is generally shortened in GC tissues compared to paracancer tissues. Moreover, KHDRBS1 mRNA with a shortened 3'UTR can escape the inhibitory effect of miRNAs, resulting in its increased expression in GC. Overexpression of KHDRBS1, especially KHDRBS1 with a shortened 3'UTR, promotes the growth and metastasis of GC in vivo and in vitro. In conclusion, the experimental results show that shortening of the KHDRBS1 mRNA 3'UTR can mediate the overexpression of KHDRBS1 in GC cells and promote the progression of GC.
Indexed as
Identifiers
36247240PMC9556470W4306667601What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.