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LncRNA HCP5: A key regulator of tumor metabolic reprogramming, signaling pathway modulation, and therapeutic
Cheng Peng1, Fang Zhang2, Fei Zhou2
1Department of Otorhinolaryngology, Hengyang First People's Hospital, Hengyang, 421002, Hunan Province, China.
Abstract:
Long non-coding RNA (lncRNA) HCP5 has emerged as a critical oncogenic regulator aberrantly expressed in multiple cancer types. This review summarizes the multifaceted roles of HCP5 in tumor progression and therapeutic resistance. Through its competitive endogenous RNA (ceRNA) activity, HCP5 sponges various microRNAs (miRNAs), thereby derepressing downstream oncogenes and activating key signaling pathways such as Wnt/β-catenin, Notch1, Hippo, and AMPK/PGC1α. These interactions collectively promote tumor cell proliferation, migration, invasion, and evasion of apoptosis. In gastric cancer and triple-negative breast cancer, HCP5 also contributes to metabolic reprogramming by enhancing fatty acid oxidation and regulating ferroptosis via its encoded peptide HCP5-132aa, respectively. Furthermore, HCP5 facilitates chemotherapy and radiotherapy resistance by modulating ABCB1 expression, DNA repair pathways, and cell cycle regulators. Overall, HCP5 functions as a central node linking oncogenic signaling, metabolic adaptation, and treatment resistance, underscoring its potential as a biomarker and therapeutic target. Continued exploration of HCP5-mediated regulatory networks may offer novel insights for precision oncology.
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