MicroRNA-29s could target AKT2 to inhibit gastric cancer cells invasion ability
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Published on: September 15, 2023
Hongkai Zhang1, Yin Cheng, Congwei Jia
1Department of Pathology, Peking Union Medical College Hospital, CAMS & PUMC, Beijing, 100730, People's Republic of China.
Abstract:
AKT2 is a crucial mediator in the tumorigenesis and thought to be an ideal target for the treatment of malignancies. Increasing evidence has also shown that microRNAs (miRNAs) could regulate or be regulated by mRNAs and they also might serve as therapeutic agencies or targets. MiR-29s (miR-29a, miR-29b and miR-29c) had been approved that they decreased in gastric cancers (GC) by targeting CCND2, MMP2 and p42.3. However, whether miR-29s would target AKT2 have not been investigated in GC. Here, we explored the relationship between miR-29s and AKT2 and found that in GC cell lines (HGC-27 and MGC-803) and GC clinical samples the decreased levels of miR-29s accompanied by increased AKT2 expression. Introduction of miR-29s into GC cells resulted in decreased AKT2 expression and decreased the ability of cancer cells invasion, so did the siRNA-AKT2. Our studies revealed that miR-29s expression is downregulated in GC and they could repress the AKT2 expression and the inactivation of AKT and GSK3beta leading to inhibit the GC cells invasion. Taken together, our findings suggested that AKT2 may be one of the targets of miR29s in gastric cancer. By increasing the expression of miR-29s or decreasing AKT2 expression may be promising in combating with GC.
Insights
MicroRNAs (miRNAs) targeting AKT2 may inhibit gastric cancer (GC) invasion. Decreased miR-29 levels correlate with increased AKT2 in GC, suggesting miR-29s as potential therapeutic agents against this malignancy.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- AKT2 is implicated in tumorigenesis and is a target for cancer treatment.
- MicroRNAs (miRNAs) are regulators of gene expression and potential therapeutic targets.
- MiR-29s are downregulated in gastric cancer (GC) and target other genes, but their role with AKT2 in GC is unexplored.
Purpose of the Study:
- To investigate the relationship between miR-29s and AKT2 in gastric cancer.
- To determine if miR-29s regulate AKT2 expression and affect GC cell invasion.
- To explore the therapeutic potential of modulating miR-29s or AKT2 in GC.
Main Methods:
- Analysis of miR-29s and AKT2 expression in GC cell lines (HGC-27, MGC-803) and clinical samples.
- Introduction of miR-29s into GC cells and assessment of AKT2 expression and cell invasion.
- Utilizing siRNA targeting AKT2 to evaluate its effect on GC cell invasion.
Main Results:
- Decreased miR-29s levels were observed alongside increased AKT2 expression in GC cell lines and samples.
- Restoring miR-29s in GC cells led to reduced AKT2 expression and decreased cancer cell invasion.
- Silencing AKT2 with siRNA also inhibited GC cell invasion, mirroring the effect of miR-29s.
Conclusions:
- MiR-29s expression is downregulated in gastric cancer.
- MiR-29s repress AKT2 expression, leading to inactivation of AKT and GSK3beta, thereby inhibiting GC cell invasion.
- Targeting AKT2 or upregulating miR-29s shows promise for combating gastric cancer.
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