Prof. Tong Zhou | Publications & Academic Profile | SinoBioData

Research Publications & English Decoded Briefs

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Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2024130

EEPD1 attenuates radiation-induced cardiac hypertrophy and apoptosis by degrading FOXO3A in cardiomyocytes

Radiation-induced heart disease (RIHD) is a severe delayed complication of thoracic irradiation (IR). Endonuclease/exonuclease/phosphatase family domain-containing 1 (EEPD1) plays an important role in DNA damage repair, but its role in RIHD is less known. In this study, EEPD1 global knockout mice, C57BL/6J mice, and C57BL/6J mice overexpressing EEPD1 are treated with radiation at a total dose of 20 Gy or 0 Gy. After 9 weeks, echocardiography is used to assess cardiac hypertrophy and apoptosis. The results show that EEPD1 deletion exacerbates radiation-induced cardiac hypertrophy and apoptosis, while EEPD1 overexpression has the opposite effect. Further mechanistic investigations reveal that EEPD1 interacts with FOXO3A and destabilizes it by catalyzing its deubiquitination. Inhibition of FOXO3A ameliorates cardiac hypertrophy and apoptosis after EEPD1 knockdown. Thus, EEPD1 protects against radiation-induced cardiac hypertrophy and apoptosis via destabilization of FOXO3A, which may offer new insight into therapeutic strategies for RIHD.

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Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025141

LINC00114 promotes colorectal cancer metastasis by targeting HNRNPA1 to regulate glutamine metabolism reprogramming and angiogenesis

Colorectal cancer (CRC) is a common type of gastrointestinal malignancy, and it has a close connection with long noncoding RNAs (lncRNAs). This study aims to examine the involvement of long noncoding RNA LINC00114, which targets heterogeneous nuclear ribonucleoprotein A1 (HNRNPA1) in regulating glutamine metabolism and angiogenesis in the metastasis of colorectal cancer (CRC). LINC00114 and HNRNPA1 levels are measured in CRC tissues and cells to determine their expression levels. Then, siRNA targeting LINC00114 (si-LINC00114) is used to transfect CRC cells, and cell proliferation and metastasis are detected. The influence of exogenous glucose and glutamine supplementation on angiogenesis induced by LINC00114 in CRC is investigated in HUVECs. Glutamine metabolism in CRC cells is also detected. Furthermore, the role of LINC00114 in CRC xenograft tumors is studied in vivo. LINC00114 and HNRNPA1 are highly expressed in CRC and positively correlate with CD31. si-LINC00114 significantly inhibits proliferation, metastasis and HNRNPA1 expression in CRC cells. An RNA-binding-protein immunoprecipitation (RIP) assay confirms that LINC00114 can bind to HNRNPA1 and positively regulate its expression. Further experiments confirm that si-LINC00114 significantly inhibits cell proliferation and tubule formation in HUVECs. Exogenous glucose and glutamine supplementation significantly promotes the levels of LINC00114 and HNRNPA1 in CRC cells and promotes tubule formation in HUVECs. In addition, transfection of CRC cells with si-LINC00114 and/or oe-HNRNPA1 regulates glutamine metabolism in CRC cells. Animal studies confirm that intervention with LINC00114 represses the progression and vascular normalization of CRC and regulates glutamine metabolism. In conclusion, LINC00114 promotes CRC metastasis by targeting HNRNPA1 to regulate glutamine metabolic reprogramming and angiogenesis.

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Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025141

LINC00114 Promotes Colorectal Cancer Metastasis by Targeting HNRNPA1 to Regulate Glutamine Metabolism Reprogramming and Angiogenesis

Colorectal cancer (CRC) remains the third most common malignancy and second leading cause of cancer-related mortality, with metastasis accounting for the majority of deaths. Long noncoding RNAs (lncRNAs) have emerged as critical regulators of tumor progression, yet the mechanistic basis of their involvement in CRC metabolic reprogramming and angiogenesis is incompletely defined. This study investigates the role of LINC00114 in CRC metastasis, focusing on its interaction with heterogeneous nuclear ribonucleoprotein A1 (HNRNPA1) and downstream effects on glutamine metabolism and angiogenesis. LINC00114 and HNRNPA1 were found to be highly expressed in CRC tissues and cells, positively correlating with CD31. siRNA-mediated silencing of LINC00114 (si-LINC00114) significantly inhibited CRC cell proliferation, metastasis, and HNRNPA1 expression. RNA-binding protein immunoprecipitation confirmed direct binding of LINC00114 to HNRNPA1, with positive regulation of HNRNPA1 expression. In HUVECs, si-LINC00114 suppressed proliferation and tubule formation. Exogenous glucose and glutamine supplementation promoted LINC00114 and HNRNPA1 levels in CRC cells and enhanced HUVEC tubule formation, with glutamine exerting a greater effect than glucose. Transfection with si-LINC00114 and/or oe-HNRNPA1 modulated glutamine metabolism in CRC cells. In vivo, LINC00114 intervention repressed tumor progression, vascular normalization, and glutamine metabolism. These findings establish LINC00114 as a promoter of CRC metastasis through HNRNPA1-mediated glutamine metabolic reprogramming and angiogenesis, suggesting potential therapeutic targets.

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