ArticleJournal of cancer research and clinical oncology2024
Upregulated lncRNA LINC01128 in colorectal cancer accelerates cell growth and predicts malignant prognosis through sponging miR-363-3p.
Article in Journal of cancer research and clinical oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- LncRNA LINC01128 promotes prostate cancer cell proliferation, metastasis, and epithelial-mesenchymal transition by modulating miR-27b-3p.Journal of cancer research and clinical oncology · 2025Article
- Long non-coding RNAs promote colorectal cancer development through other epigenetic modifications.Gastroenterology report · 2025Review
- Establishment of potential lncRNA-related hub genes involved competitive endogenous RNA in lung adenocarcinoma.BMC cancer · 2024Article
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Authors and funding
5 authors.
Funding
Abstract
purposeColorectal cancer (CRC) refers to high-mortality tumors arising in the colon or rectum with a high rate of recurrence. The involvement of long non-coding RNAs (lncRNAs) contributes to the treatment and prognosis evaluation of CRC, and brings a new direction for the radical cure of patients. To identify the pathological mechanism and regulation of lncRNA LINC01128 (LINC01128) on CRC cells, and analyze its potential prognostic value.
methodsLINC01128 level in tissue and cell specimens from 122 CRC patients was evaluated by RT-qPCR. The clinical significance and prognostic value of LINC01128 in CRC were analyzed via Kaplan-Meier and Cox analysis. CCK8 and Transwell assays were used to study the function of LINC01128 in vitro. The relationship between LINC01128 and miR-363-3p was confirmed by luciferase reporter gene assay.
resultsThe overexpression of LINC01128 is associated with TNM stage and lymph node metastasis in CRC patients. Silencing LINC01128 inhibited the proliferation and metastasis of CRC cells. In addition, LINC01128 directly targeted and negatively regulated the miR-363-3p expression, while miR-363-3p inhibitor restored the inhibitory function of LINC01128.
conclusionAs an independent prognostic factor of CRC, upregulation of LINC01128 predicts poor prognosis and accelerates tumor deterioration through miR-363-3p.
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