ArticleCancer cell international2019
miR-100-3p inhibits cell proliferation and induces apoptosis in human gastric cancer through targeting to BMPR2.
Article in Cancer cell international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- The interplay of the microbiome, host genetics, and epigenetic modifications in gastric cancer.Frontiers in microbiology · 2026Review
- Role and potential mechanisms of miR‑100 in different diseases (Review).Oncology reports · 2025Review
- Small Extracellular Vesicles Orchestrate Cisplatin-Induced Ototoxicity: Potential Biomarker and Targets Discovery.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- miR‑100: A key tumor suppressor regulatory factor in human malignant tumors (Review).International journal of molecular medicine · 2025Review
- Review
- Utilization of miRNAs as Biomarkers for the Diagnosis, Prognosis, and Metastasis in Gynecological Malignancies.International journal of molecular sciences · 2024Review
- Role of non-coding RNAs as new therapeutic targets in regulating the EMT and apoptosis in metastatic gastric and colorectal cancers.Cell cycle (Georgetown, Tex.) · 2023Review
- miR-4739/ITGA10/PI3K signaling regulates differentiation and apoptosis of osteoblast.Regenerative therapy · 2022Article
- PPDPF promotes lung adenocarcinoma progression via inhibiting apoptosis and NK cell-mediated cytotoxicity through STAT3.Oncogene · 2022Article
- Circular RNA (circ)_0129047 upregulates bone morphogenetic protein receptor type 2 expression to inhibit lung adenocarcinoma progression by sponging microRNA (miR)-1206.Bioengineered · 2022Article
- miR-3178 as a prognostic indicator and tumor suppressor of gastric cancer.Irish journal of medical science · 2022Article
- Establishment of a molecular risk model for the prognosis of cervical cancer based on microRNA expression.Annals of translational medicine · 2022Article
- Determining The Role of MicroRNAs in Self-Renewal, Metastasis and Resistance to Drugs in Human Gastric Cancer Based on Data Mining Approaches: A Systematic Review.Cell journal · 2022Review
- Article
- Hsa-miR-100-3p Controls the Proliferation, DNA Synthesis, and Apoptosis of Human Sertoli Cells by Binding to SGK3.Frontiers in cell and developmental biology · 2021Article
- miR-100 Suppresses the Proliferation, Invasion, and Migration of Hepatocellular Carcinoma Cells via Targeting CXCR7.Journal of immunology research · 2021Observational
- Article
- miR-188-5p Promotes Tumor Growth by Targeting CD2AP Through PI3K/AKT/mTOR Signaling in Children with Acute Promyelocytic Leukemia.OncoTargets and therapy · 2020Article
- LINC00319-Mediated miR-3127 Repression Enhances Bladder Cancer Progression Through Upregulation of RAP2A.Frontiers in genetics · 2020Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundmiR-100 has been reported to closely associate with gastric cancer (GC) initiation and progression. However, the underlying mechanism of miR-100-3p in GC is still largely unclear. In this study, we intend to study how miR-100-3p regulates GC malignancy.
methodsThe expression levels of miR-100-3p in vitro (GES-1 and GC cell lines) and in vivo (cancerous and normal gastric tissues) were examined by quantitative real-time PCR (qRT-PCR). MTT and PE/Annexin V analyses were responsible for measurement of the effects of miR-100-3p on GC cell proliferation and apoptosis. Transwell assay with or without matrigel was used to examine the capacity of migration and invasion in GC cells. The interaction of miR-100-3p with bone morphogenetic protein receptor 2 (BMPR2) was confirmed through transcriptomics analysis and luciferase reporter assay. qRT-PCR and Western blot analyses were applied to determine the expression of ERK/AKT and Bax/Bcl2/Caspase3, which were responsible for the dysfunction of miR-100-3p.
resultsmiR-100-3p was down-regulated in GC cell lines and cancerous tissues, and was negatively correlated with BMPR2. Loss of miR-100-3p promoted tumor growth and BMPR2 expression. Consistently, the effects of miR-100-3p inhibition on GC cells were partially neutralized by knockdown of BMPR2. Over-expression of miR-100-3p simultaneously inhibited tumor growth and down-regulated BMPR2 expression. Consistently, over-expression of BMPR2 partially neutralized the effects of miR-100-3p over-expression. Further study demonstrated that BMPR2 mediated the effects downstream of miR-100-3p, which might indirectly regulate ERK/AKT and Bax/Bcl2/Caspase3 signaling pathways.
conclusionmiR-100-3p acted as a tumor-suppressor miRNA that down-regulated BMPR2, which consequently inhibited the ERK/AKT signaling and activated Bax/Bcl2/Caspase3 signaling. This finding provided novel insights into GC and could contribute to identify a new diagnostic and therapeutic target.
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