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Updated: Jan 20, 2026
In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Cisplatin decreases cyclin D2 expression via upregulating miR‑93 to inhibit lung adenocarcinoma cell growth
Ning Xie1, Yuan-Rong Liu2, Yan-Mei Li1
1Department of Chest Surgery, Yantaishan Hospital, Yantai, Shandong 264000, P.R. China.
Abstract:
MicroRNAs (miRNAs/miRs) serve important roles in the chemotherapeutic effect of anticancer drugs. To investigate the roles of miRNAs in cisplatin‑induced suppression of lung adenocarcinoma cell proliferation, A549 cells were treated with different concentrations of cisplatin. An MTT assay demonstrated that cisplatin inhibited A549 cell proliferation in a dose‑dependent manner. Cisplatin induced cell apoptosis and inhibited cell migration by increasing the levels of miR‑93, miR‑26a and miR‑26b. Furthermore, as an upstream factor, miR‑93 was proposed to regulate cyclin D2 expression in miR‑93‑transfected A549 cells. Cisplatin also induced Bcl‑2‑associated X protein expression, and decreased that of Bcl‑2 and c‑Myc in lung adenocarcinoma cells. In vivo analysis further supported that cisplatin inhibited lung adenocarcinoma cell growth by regulating cyclin D2 and miR‑93 expression. In conclusion, our findings demonstrated that cisplatin could effectively inhibit lung adenocarcinoma cell proliferation by decreasing cyclin D2 expression via miR‑93.
Insights
Cisplatin inhibits lung adenocarcinoma cell proliferation by downregulating cyclin D2 expression through microRNA-93 (miR-93). This study reveals miR-93
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- MicroRNAs (miRNAs) are crucial in the efficacy of anticancer drugs.
- Understanding miRNA roles in lung adenocarcinoma chemoresistance is vital.
Purpose of the Study:
- To investigate the role of miRNAs in cisplatin-induced suppression of lung adenocarcinoma cell proliferation.
- To elucidate the mechanism of action for cisplatin in lung adenocarcinoma.
Main Methods:
- A549 lung adenocarcinoma cells were treated with varying cisplatin concentrations.
- MTT assays were used to assess cell proliferation.
- Apoptosis, migration, and protein expression (Bcl-2, c-Myc, cyclin D2) were analyzed.
- In vivo studies were conducted to validate findings.
Main Results:
- Cisplatin inhibited A549 cell proliferation and migration in a dose-dependent manner.
- Cisplatin increased miR-93, miR-26a, and miR-26b levels, inducing apoptosis.
- miR-93 was identified as a regulator of cyclin D2 expression.
- Cisplatin treatment decreased Bcl-2 and c-Myc, while increasing Bcl-2-associated X protein.
Conclusions:
- Cisplatin effectively inhibits lung adenocarcinoma cell proliferation.
- The mechanism involves cisplatin-induced upregulation of miR-93, leading to decreased cyclin D2 expression.
- This highlights a novel therapeutic pathway involving miR-93 and cyclin D2 in lung cancer treatment.
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