Autophagy, as a type II programmed cell death, plays crucial roles with autophagy-related (ATG) proteins in cancer. Up to now, the dual role of autophagy both in cancer progression and inhibition remains controversial, in which the numerous ATG proteins and their core complexes including ULK1/2 kinase core complex, autophagy-specific class III PI3K complex, ATG9A trafficking system, ATG12 and LC3 ubiquitin-like conjugation systems, give multiple activities of autophagy pathway and are involved in autophagy initiation, nucleation, elongation, maturation, fusion and degradation. Autophagy plays a dynamic tumor-suppressive or tumor-promoting role in different contexts and stages of cancer development. In the early tumorigenesis, autophagy, as a survival pathway and quality-control mechanism, prevents tumor initiation and suppresses cancer progression. Once the tumors progress to late stage and are established and subjected to the environmental stresses, autophagy, as a dynamic degradation and recycling system, contributes to the survival and growth of the established tumors and promotes aggressiveness of the cancers by facilitating metastasis. This indicates that regulation of autophagy can be used as effective interventional strategies for cancer therapy.

中文翻译：

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癌症中的自噬和自噬相关蛋白。

自噬作为II型程序性细胞死亡，在癌症中与自噬相关（ATG）蛋白起着至关重要的作用。迄今为止，自噬在癌症进展和抑制中的双重作用仍然存在争议，其中众多的ATG蛋白及其核心复合物包括ULK1 / 2激酶核心复合物，自噬特异性III类PI3K复合物，ATG9A转运系统，ATG12和LC3泛素样结合系统，具有多种自噬途径的活性，并参与自噬的起始，成核，延伸，成熟，融合和降解。自噬在癌症发展的不同环境和阶段中起着动态抑制肿瘤或促进肿瘤的作用。在早期肿瘤发生中，自噬作为一种生存途径和质量控制机制，可以防止肿瘤的发生并抑制癌症的进展。一旦肿瘤进展到晚期并被建立并受到环境压力，自噬作为动态降解和再循环系统，将有助于已建立肿瘤的存活和生长，并通过促进转移而促进癌症的侵袭性。这表明自噬的调节可用作癌症治疗的有效干预策略。