Obesity, a global epidemic, is an independent risk factor for the occurrence and development of a variety of tumorigenesis, such as breast cancer, pancreatic cancer, ovarian cancer and colorectal cancer. Adipocytes are important endocrine cells in the tumor microenvironment of obesity-related tumors, which can secrete a variety of adipokines (such as leptin, adiponectin, estrogen, resistin, MIF and MCP-1, etc.), among which leptin, adiponectin and estrogen are the most in-depth and valuable ones. These adipokines are closely related to tumorigenesis and the progression of tumors. In recent years, more and more studies have shown that under chronic inflammatory conditions such as obesity, adipocytes secrete more adipokines to promote the tumorigenesis and development of tumors. However, it is worth noting that although adiponectin is also secreted by adipocytes, it has an anti-tumor effect, and can cross-talk with other adipokines (such as leptin and estrogen) and insulin to play an anti-tumor effect together. In addition, obesity is the main cause of insulin resistance, which can lead to the increase of the expression levels of insulin and insulin-like growth factor (IGF). As important regulators of blood glucose and lipid metabolism, insulin and IGF also play an important role in the progress of obesity related tumors. In view of the important role of adipokines secreted by adipocytes and insulin/IGF in tumors, this article not only elaborates leptin, adiponectin and estrogen secreted by adipocytes and their mechanism of action in the development of obesity- related tumors, but also introduces the relationship between insulin/IGF, a regulator of lipid metabolism, and obesity related tumors. At the same time, it briefly describes the cancer-promoting mechanism of resistin, MIF and MCP-1 in obesity-related tumors, and finally summarizes the specific treatment opinions and measures for various adipokines and insulin/insulin-like growth factors in recent years.

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ObjectiveStudy the possible mechanism and delayed effect of tilapia skin collagen on skin aging for mice.Materials and MethodsKunming (KM) mice were randomly divided into the aging model group, the normal group, the positive control group (vitamin E) and the low, medium, high dose tilapia skin collagen groups (2.0, 4.0, 8.0 mg/g). The normal group was only injected with saline at the back and the neck. The other groups were injected subcutaneously with 5% D‐galactose and ultraviolet light jointly to establish the aging model. After modeling, the positive control group was treated with a dose of 10% vitamin E once a day, and the low, medium, high dose tilapia skin collagen group was separately applied 2.0, 4.0, 8.0 mg/g of tilapia skin collagen for 40 days. The changes of skin tissue morphology, water content, hydroxyproline (Hyp) content, and superoxide dismutase (SOD) activity in mice were studied at the day 10, 20, 30, 40, 50.ResultsCompared with the normal group, the skin of mice in the aging model group was thinner, looser, and the skin moisture content, Hyp content, SOD activity were all decreased. For mice of the low, medium, high dose tilapia skin collagen group, the thickness of dermis increased, possessing close arrangement, and the moisture content, Hyp content, SOD activity were up‐regulated significantly, which effectively alleviated the aging process of skin. The dose of tilapia skin collagen was directly proportional to the anti‐aging effect.ConclusionsTilapia skin collagen has an obvious effect on improving skin aging.

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N6-methyladenosine (m6A) modification, as the most common and abundant type of RNA modification in mammalian cells, participates in the processes of mRNA transcription, translation, splicing and degradation, serving to regulate RNA stability. In recent years, a large number of studies have indicated that m6A modification is able to affect tumor progression, participate in tumor metabolism, regulate tumor cell ferroptosis and change the tumor immune microenvironment, thereby affecting tumor immunotherapy. In the current review, the main features of m6A-associated proteins are presented with a focus on the mechanisms underpinning their roles in tumor progression, metabolism, ferroptosis and immunotherapy, also emphasizing the potential of targeting m6A-associated proteins as a promising strategy for the treatment of cancer. Contents1. Introduction 2. N6-methyladenosine (m6A) modifications 3. Targeting m6A in tumor growth and metastasis 4. Targeting m6A in tumor metabolism 5. Targeting m6A in ferroptosis 6. Targeting m6A in tumor immunotherapy 7. Potential clinical applications for targeting m6A-associated proteins 8. Conclusions and future prospects