Decoding the role of inflammation-related microRNAs in cancer cachexia: a study using HPV16-transgenic mice and in silico approaches

Santos, Julia M.; Silva, Sara Peixoto da; Bastos, Margarida M. S. M.; Oliveira, Paula A.; Costa, R.M. Gil da; Medeiros, Rui

doi:10.1007/s13105-021-00866-1

Cited by 2 publications

(2 citation statements)

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“…Recent studies related exosomal miR-155 to cancer cachexia development. Exosomal miR-155 released by BC cells facilitated beige/brown differentiation and reprogrammed metabolism in adipocytes by suppressing PPARγ expression ( 13 ). Although this work highlighted the role of exosomal miR-155 in the switch from white adipose to brown adipose, the mechanisms underpinning this effect had not been explored.…”

Section: Discussionmentioning

confidence: 99%

“…miR-155 deletion in high-fat-diet-fed mice limited inflammation in white adipose tissue and promoted adipogenesis, insulin sensitivity and energy uncoupling ( 19 ). In addition, miR-155 was reported to participate in several processes related to muscle wasting in HPV16 transgenic mice, such as muscle structure development and regulation of MAPK pathway ( 13 ). As the findings of the previous studies indicate that miR-155 exerts a pro-inflammatory effect and affects muscle wasting in white adipose, future studies are warranted to validate the effects of exosomal miR-155 on white adipocyte inflammation and muscle wasting in BC-associated cachexia.…”

Section: Discussionmentioning

confidence: 99%

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Breast cancer cell-derived exosome-delivered microRNA-155 targets UBQLN1 in adipocytes and facilitates cancer cachexia-related fat loss

Sun

Wang

Yao

et al. 2023

Human Molecular Genetics

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Cachexia occurrence and development are associated with loss of white adipose tissues, which may be involved with cancer-derived exosomes. This study attempted to characterize the functional mechanisms of bc cell-derived exosomes-loaded microRNA (miR)-155 in cancer cachexia-related fat loss. Exosomes were incubated with preadipocytes and cellular lipid droplet accumulation was observed using oil red O staining. Western blots evaluated the cellular levels of lipogenesis marker peroxisome proliferator activated receptor gamma (PPARγ) and adiponectin, C1Q and collagen domain containing (AdipoQ). Differentiated adipocytes were incubated with exosomes, and phosphate hormone sensitive lipase (P-HSL), adipose triglyceride lipase (ATGL), and glycerol were detected in adipocytes, in addition to uncoupling protein 1 (UCP1) and leptin levels. A mouse model of cancer cachexia was established where cancer exosomes were injected intravenously. The changes in body weight and tumor-free body weights were recorded and serum glycerol levels and lipid accumulation in adipose tissues were determined. Also, the relationship between miR-155 and UBQLN1 was predicted and verified. bc exosome treatment reduced PPARγ and AdipoQ protein levels, promoted the levels of P-HSL and ATGL proteins, facilitated glycerol release, increased UCP1 expression, and lowered leptin expression in adipocytes. Exosomal miR-155 inhibited lipogenesis in preadipocytes and boosted the browning of white adipose tissues. miR-155 downregulation alleviated cancer exosome-induced browning of white adipose tissues and fat loss. Mechanistically, miR-155 targeted UBQLN1, and UBQLN1 upregulation reversed the impacts of cancer exosomes. miR-155 loaded by bc cell-derived exosomes significantly affects white adipose browning and inhibition of cancer-derived exosomes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%