miR‐6844/HSD17B13 Axis Contributes the Malignant Phenotype of Hepatocellular Carcinoma Cells

Hepatocellular carcinoma (HCC) is a prevalent form of primary liver cancer, and aberrant miRNAs expression significantly contributes to its progression. Although the abnormal expression of miR-6844 in HCC has been reported, its impact on the malignant phenotype of HCC cells and its potential mechanism remains unclear. In this study, we initially conducted a bioinformatics analysis to investigate the differential expression of miR-6844 in HCC tissues and its impact on patient prognosis. The association between miR-6844 expression levels and clinical characteristics of HCC patients was subsequently investigated by integrating data from clinical samples. Ultimately, the impact of miR-6844 on the malignant phenotype of HCC cells and the underlying mechanisms were examined through in vitro cellular experiments. The results showed that a high expression of miR-6844 in HCC, which was associated with poor prognosis and exhibited significant correlations with intrahepatic metastasis and clinical stage among patients. The upregulation of miR-6844 promoted the proliferation, migration, and invasion of HCC cells while suppressing apoptosis. Conversely, the downregulation of miR-6844 significantly attenuated the malignant phenotype of HCC cells. In addition, HSD17B13 was identified as a target gene of miR-6844, and the overexpression of HSD17B13 partially counteracted the oncogenic effects induced by miR-6844 in HCC cells, otherwise the opposite. Taken together, the above results suggest that miR-6844 plays a regulatory role in the malignant phenotype of HCC cells through its targeting of HSD17B13.

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Journal
Cell Biology International
Published
2025-04-21
DOI
https://doi.org/10.1002/cbin.70025
Citations
1
Primary Topic
MicroRNA in disease regulation
Type
article
Field-Weighted Citation Impact
0.94
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article

miR‐6844/HSD17B13 Axis Contributes the Malignant Phenotype of Hepatocellular Carcinoma Cells

Li Liao, Qilin Yi, Xu Ming, Yu Liu et al.
1 citations
Cell Biology International
MicroRNA in disease regulation
0.94
article

miR‐6844/HSD17B13 Axis Contributes the Malignant Phenotype of Hepatocellular Carcinoma Cells

Li Liao, Qilin Yi, Xu Ming, Yu Liu, Shuai Chen, Zhen Zhao, Tao Wu
article en
1 citations

Abstract

Hepatocellular carcinoma (HCC) is a prevalent form of primary liver cancer, and aberrant miRNAs expression significantly contributes to its progression. Although the abnormal expression of miR-6844 in HCC has been reported, its impact on the malignant phenotype of HCC cells and its potential mechanism remains unclear. In this study, we initially conducted a bioinformatics analysis to investigate the differential expression of miR-6844 in HCC tissues and its impact on patient prognosis. The association between miR-6844 expression levels and clinical characteristics of HCC patients was subsequently investigated by integrating data from clinical samples. Ultimately, the impact of miR-6844 on the malignant phenotype of HCC cells and the underlying mechanisms were examined through in vitro cellular experiments. The results showed that a high expression of miR-6844 in HCC, which was associated with poor prognosis and exhibited significant correlations with intrahepatic metastasis and clinical stage among patients. The upregulation of miR-6844 promoted the proliferation, migration, and invasion of HCC cells while suppressing apoptosis. Conversely, the downregulation of miR-6844 significantly attenuated the malignant phenotype of HCC cells. In addition, HSD17B13 was identified as a target gene of miR-6844, and the overexpression of HSD17B13 partially counteracted the oncogenic effects induced by miR-6844 in HCC cells, otherwise the opposite. Taken together, the above results suggest that miR-6844 plays a regulatory role in the malignant phenotype of HCC cells through its targeting of HSD17B13.

Cell Biology InternationalVol. 49(7)
Yueyang Second People's Hospital (CN)
No poverty
Openalex Percentile: Top 26%
MicroRNA in disease regulation
0.94
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