ArticleOncology letters2021
lncRNA MT1JP-overexpression abolishes the silencing of PTEN by miR-32 in hepatocellular carcinoma.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Resistance of first-line targeted drugs in hepatocellular carcinoma: the epigenetic regulation mechanisms.Cell death & disease · 2025Review
- Screening and validation of long non-coding RNAs associated with colorectal cancer based on random forest and LASSO regression algorithm.Discover oncology · 2025Article
- MT1JP: A Pivotal Tumor-Suppressing LncRNA and its Role in Cancer Progression and Therapeutic Potential.Current drug targets · 2025Review
- The functions of long noncoding RNAs on regulation of F-box proteins in tumorigenesis and progression.Frontiers in oncology · 2022Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have shown that long non-coding RNA (lncRNA) MT1JP plays a role as a tumor suppressor in several types of cancer. The present study aimed to explore the role of MT1JP in hepatocellular carcinoma (HCC). Paired HCC and non-tumor tissues from 64 patients with HCC were subjected to RNA isolation and reverse transcription-quantitative PCR (RT-qPCR) to analyze the differential expression of MT1JP, microRNA (miR)-32 and phosphatase and tensin homolog (PTEN) in HCC. Cell transfections, followed by RT-qPCR and western blotting, were carried out to investigate the interactions among MT1JP, miR-32 and PTEN. The role of MT1JP, miR-32 and PTEN in regulating HCC cell proliferation was assessed using a Cell Counting Kit-8 assay. It was found that MT1JP was downregulated in HCC cancer tissues compared with that in non-cancer tissues. Survival analysis showed that patients with low MT1JP expression levels exhibited a significantly higher 5-year overall survival rate compared with patients with high MT1JP levels. The expression of MT1JP in HCC tissues was positively associated with PTEN and negatively associated with miR-32. Overexpression of MT1JP increased the expression levels of PTEN and decreased the expression levels of miR-32. Overexpression of miR-32 did not affect the expression of MT1JP but decreased the expression levels of PTEN and attenuated the effect of overexpression of MT1JP on the expression of PTEN. Overexpression of MT1JP and PTEN decreased the proliferation of HCC cells. Overexpression of miR-32 played an opposite role and attenuated the effects of overexpression of MT1JP. Therefore, MT1JP may upregulate PTEN by downregulating miR-32 to regulate HCC cell proliferation.
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