ArticleOncology letters2020
Mechanism of miR-98 inhibiting tumor proliferation and invasion by targeting IGF1R in diabetic patients combined with colon cancer.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Screening and predictive analysis of common regulatory genes in diabetes and rectal cancer: transcriptional and drug modulation mechanisms.European journal of medical research · 2025Article
- Bta-Let-7d Modulation of Oxidative Stress Induced by Potassium Permanganate in Bovine Endometrial Cells via IGF1R/PI3K/AKT Signaling Pathway.Antioxidants (Basel, Switzerland) · 2025Article
- MicroRNA-98: the multifaceted regulator in human cancer progression and therapy.Cancer cell international · 2024Review
- BZW2 Inhibition Reduces Colorectal Cancer Growth and Metastasis.Molecular cancer research : MCR · 2023Article
- The Insulin-like Growth Factor System and Colorectal Cancer.Life (Basel, Switzerland) · 2022Review
- [Dihydromyricetin reverses Herceptin resistance by up-regulating miR-98-5p and inhibiting IGF1R/HER2 dimer formation in SKBR3 cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Exosomes derived from microRNA-129-5p-modified tumor cells selectively enhanced suppressive effect in malignant behaviors of homologous colon cancer cells.Bioengineered · 2021Article
- Circular RNA 0006349 Augments Glycolysis and Malignance of Non-small Cell Lung Cancer Cells Through the microRNA-98/MKP1 Axis.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression level of miR-98 in diabetic colon cancer (CRC) tissues and the regulation mechanism of colon cancer cell proliferation and invasion ability were studied. Forty patients with type 2 diabetes mellitus complicated with colon cancer, 40 colon cancer patients, and 40 patients with diabetic colonoscopy were enrolled between January 2017 and January 2018. Real-time quantitative PCR was used to detect the expression level of miR-98. After SW480 cells were transfected with miR-98 mimics or control simulants, the proliferation of cancer cells was detected by MTT assay, and the invasion ability of cancer cells was detected by Transwell cell invasion assay. The dual luciferase assay was used to detect the binding relationship between miR-98 and IGF1R. Western blot analysis was used to detect the expression of IGF1R protein in tumor tissues of patients with diabetes mellitus and colon cancer. Compared with diabetic patients, the expression level of miR-98 was decreased in colon cancer patients. Compared with tumor tissues of colon cancer patients, the expression level of miR-98 was significantly decreased in diabetic colon cancer tissues. Compared with the commonly cultured colon cancer SW480 cells, the expression level of miR-98 was significantly decreased in SW480 cells cultured under high glucose conditions. Increased expression of miR-98 inhibits colon cancer cell proliferation and invasion. miR-98 can target and bind to IGF1R and inhibit its expression level. IGF1R is upregulated in diabetic colon cancer tissue. miR-98 inhibits proliferation and invasion of diabetic colon cancer by targeting IGF1R. The expression level of miR-98 in diabetic colon cancer tissues is lower than that in colon cancer tissues. miR-98 can inhibit the proliferation and invasion of colon cancer cells by targeting the target gene IGF1R. miR-98 may be a potential biological target for the treatment of patients with diabetes and colon cancer.
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