The role and function of autophagy through signaling and pathogenetic pathways and lncRNAs in ovarian cancer

Abstract

Lysosomal-driven autophagy is a tightly controlled cellular catabolic process that breaks down and recycles broken or superfluous cell parts. It is involved in several illnesses, including cancer, and is essential in preserving cellular homeostasis. Autophagy prevents DNA mutation and cancer development by actively eliminating pro-oxidative mitochondria and protein aggregates from healthy cells. Oncosuppressor and oncogene gene mutations cause dysregulation of autophagy. Increased autophagy may offer cancer cells a pro-survival advantage when oxygen and nutrients are scarce and resistance to chemotherapy and radiation. This finding justifies the use of autophagy inhibitors in addition to anti-neoplastic treatments. Excessive autophagy levels can potentially kill cells. The diagnosis and treatment of ovarian cancer present many difficulties due to its complexity and heterogeneity. Understanding the role of autophagy, a cellular process involved in the breakdown and recycling of cellular components, in ovarian cancer has garnered increasing attention in recent years. Of particular note is the increasing amount of data indicating a close relationship between autophagy and ovarian cancer. Autophagy either promotes or restricts tumor growth in ovarian cancer. Dysregulation of autophagy signaling pathways in ovarian cancers can affect the development, metastasis, and response to tumor treatment. The precise mechanism underlying autophagy concerning ovarian cancer remains unclear, as does the role autophagy plays in ovarian carcinoma. In this review, we tried to encapsulate and evaluate current findings in investigating autophagy in ovarian cancer.

Keywords: Autophagy; Epigenetic; Long non-coding RNAs; Ovarian cancer.