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Updated: May 9, 2026

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Published on: October 27, 2014
Let-7c inhibits A549 cell proliferation through oncogenic TRIB2 related factors
Ping-Yu Wang1, Yun-Xiao Sun, Shuai Zhang
1Key Laboratory of Tumor Molecular Biology in Binzhou Medical University, Department of Biochemistry and Molecular Biology, Binzhou Medical University, YanTai, ShanDong 264003, PR China.
Abstract:
MicroRNAs have tumor suppressive or oncogenic roles in carcinogenesis. This study aimed to investigate the mechanism of let-7c in suppressing lung cancer cell proliferation. First, let-7c was revealed to be able to inhibit lung adenocarcinoma cell proliferation significantly. TRIB2 was further demonstrated to be a novel target and negatively regulated by let-7c. As downstream signals of TRIB2, the activities of C/EBP-α and phosphorylated p38MAPK were increased obviously in let-7c-treated cells compared with controls. Our results demonstrate that, through regulating the expression of TRIB2 and its downstream factors, let-7c can effectively inhibit A549 cell proliferation in vitro and in vivo.
Insights
MicroRNAs, including let-7c, can suppress lung cancer. This study shows let-7c inhibits lung adenocarcinoma cell proliferation by targeting TRIB2 and affecting downstream signaling pathways.
Area of Science:
- Molecular biology
- Oncology
- Gene regulation
Background:
- MicroRNAs play crucial roles in cancer, acting as either tumor suppressors or oncogenes.
- Understanding the specific mechanisms of microRNAs in lung cancer is vital for developing targeted therapies.
Purpose of the Study:
- To elucidate the mechanism by which let-7c suppresses lung adenocarcinoma cell proliferation.
- To identify novel targets of let-7c and their downstream effects in lung cancer.
Main Methods:
- In vitro and in vivo experiments were conducted to assess the effect of let-7c on lung cancer cell proliferation.
- Target gene identification and validation were performed, including analysis of TRIB2 expression.
- Downstream signaling pathways, specifically C/EBP-α and phosphorylated p38MAPK, were investigated.
Main Results:
- let-7c significantly inhibited the proliferation of lung adenocarcinoma cells.
- TRIB2 was identified as a direct target of let-7c, with its expression being negatively regulated by let-7c.
- The activity of C/EBP-α and phosphorylated p38MAPK was notably increased in cells treated with let-7c, indicating their role as downstream effectors.
Conclusions:
- let-7c acts as a tumor suppressor in lung adenocarcinoma by inhibiting cell proliferation.
- The mechanism involves the negative regulation of TRIB2 and subsequent modulation of downstream factors like C/EBP-α and p38MAPK.
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