Cancer cells have an increased demand for energy sources to support accelerated rates of growth. When nutrients become limiting, cancer cells may switch to nonconventional energy sources that are mobilized through nutrient scavenging pathways involving autophagy and the lysosome. Thus, several cancers are highly reliant on constitutive activation of these pathways to degrade and recycle cellular materials. Here, we focus on the MiT/TFE family of transcription factors, which control transcriptional programs for autophagy and lysosome biogenesis and have emerged as regulators of energy metabolism in cancer. These new findings complement earlier reports that chromosomal translocations and amplifications involving the MiT/TFE genes contribute to the etiology and pathophysiology of renal cell carcinoma, melanoma, and sarcoma, suggesting pleiotropic roles for these factors in a wider array of cancers. Understanding the interplay between the oncogenic and stress-adaptive roles of MiT/TFE factors could shed light on fundamental mechanisms of cellular homeostasis and point to new strategies for cancer treatment.

中文翻译：

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MiT/TFE 转录因子家族、溶酶体和癌症。


癌细胞对能源的需求增加，以支持加速的生长。当营养物质变得有限时，癌细胞可能会转向通过涉及自噬和溶酶体的营养清除途径动员的非常规能源。因此，一些癌症高度依赖于这些途径的组成性激活来降解和回收细胞材料。在这里，我们重点关注 MiT/TFE 转录因子家族，它们控制自噬和溶酶体生物发生的转录程序，并已成为癌症能量代谢的调节因子。这些新发现补充了先前的报道，即涉及 MiT/TFE 基因的染色体易位和扩增导致肾细胞癌、黑色素瘤和肉瘤的病因学和病理生理学，表明这些因素在更广泛的癌症中具有多效性作用。了解 MiT/TFE 因子的致癌作用和应激适应性作用之间的相互作用可以揭示细胞稳态的基本机制，并为癌症治疗指明新策略。