Yi Yang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Yi Yang has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
- Changyun Huang
College of Life Sciences and Health, Wuhan University of Science and Technology, No. 2 Huangjiahu West Road, Hongshan District, Wuhan 430081, China
1 shared publication - Hang Min
College of Life Sciences and Health, Wuhan University of Science and Technology, No. 2 Huangjiahu West Road, Hongshan District, Wuhan 430081, China
1 shared publication - Hao Zhou
College of Life Sciences and Health, Wuhan University of Science and Technology, No. 2 Huangjiahu West Road, Hongshan District, Wuhan 430081, China
1 shared publication - Jun Zhou
College of Life Sciences and Health, Wuhan University of Science and Technology, No. 2 Huangjiahu West Road, Hongshan District, Wuhan 430081, China
1 shared publication - Lingjing Tao
College of Life Sciences and Health, Wuhan University of Science and Technology, No. 2 Huangjiahu West Road, Hongshan District, Wuhan 430081, China
1 shared publication - Wenbo Zhang
College of Life Sciences and Health, Wuhan University of Science and Technology, No. 2 Huangjiahu West Road, Hongshan District, Wuhan 430081, China
1 shared publication
Latest Publications
- Open Access
- 31 July 2026
- Published by MDPI AG in Current Issues in Molecular Biology
- Vol. 48 (8) , 784
PSPH Promotes Hepatocellular Carcinoma Progression by Upregulating HIF-1α and Is Regulated by LncRNA GSEC/miR-101-3p
Hepatocellular carcinoma (HCC) lacks effective early diagnostic markers and is heavily driven by angiogenesis and hypoxia. Emerging evidence indicates that metabolic enzymes and noncoding RNAs coordinate these processes. Here, we reveal that phosphoserine phosphatase (PSPH), a serine biosynthesis enzyme, is significantly upregulated in HCC, correlating with angiogenic markers and poor prognosis. Clinical data and functional assays demonstrated that miR-101-3p directly targets the PSPH 3′ UTR to suppress its expression, while lncRNA GSEC acts as a competing endogenous RNA to sponge miR-101-3p. In vitro, GSEC knockdown or miR-101-3p overexpression decreased PSPH and HIF1α levels, strongly inhibiting HCC angiogenesis, migration, invasion, and proliferation. Crucially, these anti-tumor effects were reversed by restoring PSPH. In vivo, modulating the GSEC/PSPH axis significantly altered xenograft tumor growth and vascularization. Conclusively, the GSEC/miR-101-3p/PSPH regulatory axis drives HIF1α-dependent angiogenesis and HCC progression, highlighting PSPH as a promising diagnostic biomarker and therapeutic target.
- 31 July 2026
- Published by MDPI AG in Current Issues in Molecular Biology
- Vol. 48 (8) , 784
Open AccessPSPH Promotes Hepatocellular Carcinoma Progression by Upregulating HIF-1α and Is Regulated by LncRNA GSEC/miR-101-3p
Hepatocellular carcinoma (HCC) lacks effective early diagnostic markers and is heavily driven by angiogenesis and hypoxia. Emerging evidence indicates that metabolic enzymes and noncoding RNAs coordinate these processes. Here, we reveal that phosphoserine phosphatase (PSPH), a serine biosynthesis enzyme, is significantly upregulated in HCC, correlating with angiogenic markers and poor prognosis. Clinical data and functional assays demonstrated that miR-101-3p directly targets the PSPH 3′ UTR to suppress its expression, while lncRNA GSEC acts as a competing endogenous RNA to sponge miR-101-3p. In vitro, GSEC knockdown or miR-101-3p overexpression decreased PSPH and HIF1α levels, strongly inhibiting HCC angiogenesis, migration, invasion, and proliferation. Crucially, these anti-tumor effects were reversed by restoring PSPH. In vivo, modulating the GSEC/PSPH axis significantly altered xenograft tumor growth and vascularization. Conclusively, the GSEC/miR-101-3p/PSPH regulatory axis drives HIF1α-dependent angiogenesis and HCC progression, highlighting PSPH as a promising diagnostic biomarker and therapeutic target.