Zinger Adar, Cho William C, Ben-Yehuda Arie
1Department of Medicine, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
2Department of Clinical Oncology, Queen Elizabeth Hospital, Kowloon, Hong Kong.
Aging Dis. 2017 Oct 1;8(5):611-627. doi: 10.14336/AD.2016.1230. eCollection 2017 Oct.
Aging and cancer are highly correlated biological phenomena. Various cellular processes such as DNA damage responses and cellular senescence that serve as tumor suppressing mechanisms throughout life result in degenerative changes and contribute to the aging phenotype. In turn, aging is considered a pro-tumorigenic state, and constitutes the single most important risk factor for cancer development. However, the causative relations between aging and cancer is not straight forward, as these processes carry contradictory hallmarks; While aging is characterized by tissue degeneration and organ loss of function, cancer is a state of sustained cellular proliferation and gain of new functions. Here, we review the molecular and cellular pathways that stand in the base of aging related cancer. Specifically, we deal with the inflammatory perspective that link these two processes, and suggest possible molecular targets that may be exploited to modify their courses.
衰老和癌症是高度相关的生物学现象。各种细胞过程,如DNA损伤反应和细胞衰老,在整个生命过程中作为肿瘤抑制机制,会导致退行性变化并促成衰老表型。反过来,衰老被认为是一种促癌状态,并且是癌症发生的最重要单一风险因素。然而,衰老与癌症之间的因果关系并非简单直接,因为这些过程具有相互矛盾的特征;衰老的特征是组织退化和器官功能丧失,而癌症是细胞持续增殖并获得新功能的状态。在这里,我们综述了与衰老相关癌症的分子和细胞途径。具体而言,我们探讨了将这两个过程联系起来的炎症视角,并提出了可能用于改变其进程的潜在分子靶点。