Tanshinone ⅡA inhibits human esophageal cancer cell growth through miR-122-mediated PKM2 down-regulation
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Hong-Sheng Zhang1, Feng-Juan Zhang1, Hu Li1
1College of Life Science & Bioengineering, Beijing University of Technology, Pingleyuan 100#, District of Chaoyang, Beijing, 100124, China.
Abstract:
Pyruvate kinase M2 (PKM2) plays a pivotal role in the growth, survival and metabolic reprogramming of cancer cells. Here, we presented for the first time that tanshinone ⅡA inhibited human esophagus cancer cell growth through miR-122-mediated PKM2 down-regulation pathway. Tanshinone ⅡA inhibited cell proliferation and induced cell cycle arrest in S phase in human Ec109 cells. As expected, tanshinone ⅡA down-regulated PKM2 mRNA and protein expression in Ec109 cells. Given these findings, we further investigated microRNAs regulation of PKM2 and confirmed miR-122 for targeting PKM2. Moreover, we found that tanshinone ⅡA-induced up-regulation of miR-122 expression inhibited PKM2 expression in Ec109 cells. Meanwhile, tanshinone ⅡA inhibited proliferation through miR122-medated PKM2 down-regulation. It was demonstrated that the anticancer activity of tanshinone ⅡA was targeted at metabolic regulation of miR-122/PKM2 in human esophagus cancer cells. Taken together, our results revealed tanshinone ⅡA targeting at PKM2-mediated metabolic reprogramming play an important role in inhibition of esophageal cancer cell growth.
Insights
Tanshinone IIA inhibits esophageal cancer cell growth by down-regulating pyruvate kinase M2 (PKM2) via miR-122. This reveals a novel therapeutic pathway targeting metabolic reprogramming in esophageal cancer.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Pyruvate kinase M2 (PKM2) is crucial for cancer cell growth, survival, and metabolic reprogramming.
- Esophageal cancer remains a significant global health challenge with a need for novel therapeutic strategies.
Purpose of the Study:
- To investigate the inhibitory effect of tanshinone IIA on human esophageal cancer cell growth.
- To elucidate the underlying molecular mechanism involving microRNA-122 (miR-122) and pyruvate kinase M2 (PKM2).
Main Methods:
- Cell proliferation assays and cell cycle analysis in Ec109 cells.
- Quantitative real-time PCR and Western blotting to assess PKM2 and miR-122 expression.
- Bioinformatic analysis and luciferase reporter assays to confirm miR-122 targeting of PKM2.
Main Results:
- Tanshinone IIA inhibited proliferation and induced S-phase arrest in Ec109 cells.
- Tanshinone IIA down-regulated PKM2 mRNA and protein expression.
- Tanshinone IIA up-regulated miR-122 expression, which directly targeted and inhibited PKM2.
- The anti-cancer effect was mediated through the miR-122/PKM2 pathway, impacting metabolic reprogramming.
Conclusions:
- Tanshinone IIA exhibits anti-esophageal cancer activity by inhibiting cell growth and proliferation.
- The mechanism involves the up-regulation of miR-122, leading to the down-regulation of PKM2.
- Targeting the miR-122/PKM2 axis and PKM2-mediated metabolic reprogramming represents a promising therapeutic strategy for esophageal cancer.
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