Arizmendi-Izazaga Adán, Navarro-Tito Napoleón, Jiménez-Wences Hilda, Mendoza-Catalán Miguel A, Martínez-Carrillo Dinorah N, Zacapala-Gómez Ana E, Olea-Flores Monserrat, Dircio-Maldonado Roberto, Torres-Rojas Francisco I, Soto-Flores Diana G, Illades-Aguiar Berenice, Ortiz-Ortiz Julio
Laboratorio de Biomedicina Molecular, Facultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Av. Lázaro Cárdenas S/N, Ciudad Universitaria, Colonia La Haciendita, Chilpancingo C.P. 39090, Guerrero, Mexico.
Laboratorio de Biología Celular del Cáncer, Facultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Av. Lázaro Cárdenas S/N, Ciudad Universitaria, Colonia La Haciendita, Chilpancingo C.P. 39090, Guerrero, Mexico.
Pathogens. 2021 Mar 16;10(3):347. doi: 10.3390/pathogens10030347.
Metabolic reprogramming is considered one of the hallmarks in cancer and is characterized by increased glycolysis and lactate production, even in the presence of oxygen, which leads the cancer cells to a process called "aerobic glycolysis" or "Warburg effect". The E6 and E7 oncoproteins of human papillomavirus 16 (HPV 16) favor the Warburg effect through their interaction with a molecule that regulates cellular metabolism, such as p53, retinoblastoma protein (pRb), c-Myc, and hypoxia inducible factor 1α (HIF-1α). Besides, the impact of the E6 and E7 variants of HPV 16 on metabolic reprogramming through proteins such as HIF-1α may be related to their oncogenicity by favoring cellular metabolism modifications to satisfy the energy demands necessary for viral persistence and cancer development. This review will discuss the role of HPV 16 E6 and E7 variants in metabolic reprogramming and their contribution to developing and preserving the malignant phenotype of cancers associated with HPV 16 infection.
代谢重编程被认为是癌症的标志之一，其特征是即使在有氧的情况下糖酵解和乳酸生成增加，这导致癌细胞进入一个被称为“有氧糖酵解”或“瓦伯格效应”的过程。人乳头瘤病毒16型（HPV 16）的E6和E7癌蛋白通过与调节细胞代谢的分子（如p53、视网膜母细胞瘤蛋白（pRb）、c-Myc和缺氧诱导因子1α（HIF-1α））相互作用，促进瓦伯格效应。此外，HPV 16的E6和E7变体通过HIF-1α等蛋白质对代谢重编程的影响，可能与其致癌性有关，因为它们有利于细胞代谢改变，以满足病毒持续存在和癌症发展所需的能量需求。本综述将讨论HPV 16 E6和E7变体在代谢重编程中的作用，以及它们对与HPV 16感染相关癌症恶性表型的发展和维持的贡献。
