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

被引:1
|
作者
Li, Pin [1 ,2 ]
Qian, Li-Heng [3 ]
Liao, Ying-Na [3 ]
Gai, Yan-Zhi [3 ]
Pan, Hong [3 ]
Han, Long [4 ]
Nie, Hui-Zhen [3 ]
机构
[1] Shanghai Jiao Tong Univ, Int Peace Matern & Child Hlth Hosp, Sch Med, Shanghai 200030, Peoples R China
[2] Shanghai Key Lab Embryo Original Dis, Shanghai 200030, Peoples R China
[3] Shanghai Jiao Tong Univ, Renji Hosp, Shanghai Canc Inst, State Key Lab Syst Med Canc,Sch Med, Shanghai 200240, Peoples R China
[4] Qingdao Univ, Women & Childrens Hosp, Qingdao 266034, Peoples R China
基金
中国国家自然科学基金;
关键词
JPT1; Ovarian cancer; mTOR; Oxidative phosphorylation; Metabolism reprogramming; STAGE-III; PACLITAXEL; CISPLATIN; HN1; PHOSPHORYLATION; CARBOPLATIN; GROWTH;
D O I
10.1007/s43032-024-01456-4
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
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.
引用
收藏
页码:1868 / 1880
页数:13
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