Objective To investigate serum adiponectin and visfatin levels, and their ratio, in patients with endometrial cancer. Methods A retrospective case–control study of 53 patients with endometrial cancer admitted to Dalian Municipal Women and Children's Medical Center, China, between May 1, 2009, and January 31, 2013. Ninety‐eight healthy women who underwent physical examination at the same time served as the control group. Serum adiponectin and visfatin levels were measured by ELISA. Results Serum adiponectin level in the endometrial cancer group was significantly lower than in the control group (2.09 ± 1.24 μg/mL vs 7.59 ± 2.29 μg/mL; P<0.001). Serum adiponectin was positively correlated with visfatin level (Spearman correlation coefficient 0.472). The visfatin:adiponectin ratio in the endometrial cancer group was significantly higher than the control group (0.28 ± 0.10 vs 0.11 ± 0.09; P=0.047). Multivariate logistic regression showed that decreased serum adiponectin (odds ratio 0.998, 95% CI 0.996–0.999; P=0.045) and increased visfatin (1.010, 1.003–1.017; P=0.042) levels were independent risk factors for the onset of endometrial cancer. Conclusion Decreased serum adiponectin or increased visfatin levels are independent risk factors for endometrial cancer. The visfatin:adiponectin ratio has a certain reference value for the diagnosis of endometrial cancer.

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Mitophagy is a vital process that controls mitochondria quality, dysregulation of which can promote cancer. Oncoprotein mucin 1 (MUC1) targets mitochondria to attenuate drug-induced apoptosis. However, little is known about whether and how MUC1 contributes to mitochondrial homeostasis in cancer cells. We identified a novel role of MUC1 in promoting mitophagy. Increased mitophagy is coupled with the translocation of MUC1 to mitochondria, where MUC1 interacts with and induces degradation of ATPase family AAA domain-containing 3A (ATAD3A), resulting in protection of PTEN-induced kinase 1 (Pink1) from ATAD3A-mediated cleavage. Interestingly, MUC1-induced mitophagy is associated with increased oncogenicity of cancer cells. Similarly, inhibition of mitophagy significantly suppresses MUC1-induced cancer cell activity in vitro and in vivo. Consistently, MUC1 and ATAD3A protein levels present an inverse relationship in tumor tissues of breast cancer patients. Our data validate that MUC1/ATAD3A/Pink1 axis-mediated mitophagy constitutes a novel mechanism for maintaining the malignancy of cancer cells, providing a novel therapeutic approach for MUC1-positive cancers.

Mitochondria are the ‘engine’ of cells. Mitochondrial dysfunction is an important mechanism in many human diseases. Many natural products could remedy the mitochondria to alleviate mitochondria-involved diseases. In this review, we summarized the current knowledge of the relationship between the mitochondria and human diseases and the regulation of natural products to the mitochondria. We proposed that the development of mitochondrial regulators/nutrients from natural products to remedy mitochondrial dysfunction represents an attractive strategy for a mitochondria-involved disorder therapy. Moreover, investigating the mitochondrial regulation of natural products can potentiate the in-depth comprehension of the mechanism of action of natural products.

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