2. Academic Validation
  3. Hematological and Neurological Expressed 1 Promotes Tumor Progression Through mTOR Signaling in Ovarian Cancer

Hematological and Neurological Expressed 1 Promotes Tumor Progression Through mTOR Signaling in Ovarian Cancer

  • Reprod Sci. 2024 Jan 23. doi: 10.1007/s43032-024-01456-4.
Pin Li # 1 2,  Li-Heng Qian # 3,  Ying-Na Liao 3,  Yan-Zhi Gai 3,  Hong Pan 3,  Long Han 4,  Hui-Zhen Nie 5
Affiliations

Affiliations

  • 1 The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200030, China.
  • 2 Shanghai Key Laboratory of Embryo Original Diseases, Shanghai, 200030, China.
  • 3 State Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200240, China.
  • 4 Women and Children's Hospital, Qingdao University, Qingdao, 266034, China. [email protected].
  • 5 State Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200240, China. [email protected].
  • # Contributed equally.
PMID: 38263477 DOI: 10.1007/s43032-024-01456-4
Abstract

Ovarian Cancer (OV) is a highly aggressive malignancy with poor prognosis due to recurrence and drug resistance. Therefore, it is imperative to investigate the key molecular mechanisms underlying OV progression in order to develop promising diagnostic and therapeutic interventions. Although the importance of hematological and neurological expressed 1 (HN1) protein in hemopoietic cell and neurological development has been well-established, its function in Cancer, particularly in OV, remains uncertain. In this study, we compared the expression of HN1 in ovarian cancers and para-tumor tissues and predicted potential related signaling pathways through enrichment analysis. In order to confirm the role of HN1 in vitro and vivo, we carried out a variety of experiments including bioinformation analysis, colony formation, flow cytometry analysis, and subcutaneous tumor models. The results demonstrated that HN1 was upregulated in OV and was negatively associated with clinical prognosis. Moreover, we observed that HN1 enhances cell proliferation, migration, and drug resistance, while suppressing Apoptosis in OV cells. Notably, we discovered that HN1 functions as a novel regulator of mTOR pathways. Our findings suggest that HN1-mediated mTOR regulation facilitates OV advancement and targeting HN1 could provide a promising therapeutic approach for clinical OV treatment.

Keywords

JPT1; Metabolism reprogramming; Ovarian cancer; Oxidative phosphorylation; mTOR.

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