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

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.

Unrevealing the vital role of ncRNAs in Gastric Cancer chemoresistance.

The high incidence of gastric cancer in many nations and poor overall survival rates has remained a serious global health concern. Chemoresistance in gastric cancer is a significant issue that hinders the efficacy of available treatment options. In gastric cancer, non-coding RNAs like microRNAs, long non-coding RNAs, and circular RNAs have become effective regulators of chemoresistance. These non-coding RNAs can influence several mechanisms, including drug efflux transporters, drug metabolism, and detoxification, cancer stem cells and the epithelial-mesenchymal transition, autophagy and apoptosis, and the tumor microenvironment. In this article review, we summarize the key roles non-coding RNAs play in the chemoresistance of gastric cancer and consider how they might be used in clinical settings as markers for diagnosis and prognosis, as well as potential targets and treatment plans. We also emphasize the need for additional study and collaborations in this area and highlight the difficulties and opportunities in non-coding RNA research for gastric cancer chemoresistance. This review offers crucial insights into the intricate relationship between non-coding RNAs and chemoresistance in gastric cancer, with implications for precision oncology and personalized medicine.