MicroRNA‑615‑5p regulates the proliferation and apoptosis of breast cancer cells by targeting HSF1

Liu, Kaisheng; Ma, Rong

doi:10.3892/etm.2021.9624

Cited by 10 publications

(5 citation statements)

References 48 publications

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“…The identification of a regulatory role of muscle HSF1 in cellular glucose metabolism provides insight into the mechanisms underlying the regulation of cellular metabolism and suggests wider application of HSF1 for targeting context-specific biological processes beyond the AMPK/ PGC-1α signaling pathway. 34 In the present study, HSF1 expression was decreased in the skeletal muscles, which attenuated the decline in insulin sensitivity associated with obesity. HSF1 activation was associated with glucose utilization by skeletal muscles.…”

Section: Discussionsupporting

confidence: 52%

Skeletal muscle HSF1 prevents insulin resistance by improving glucose utilization

Lin

et al. 2022

The FASEB Journal

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The regulation of muscle glucose utilization has significant potential for the treatment of type 2 diabetes mellitus (T2DM) and obesity. Heat shock factor 1 (HSF1) is involved in cellular metabolism and regulation of muscle metabolism. However, it is unclear how HSF1 regulates muscle glucose metabolism. In the present study, the development of obesity in mice was associated with HSF1 downregulation. Serum samples and muscle biopsies were obtained from obese and healthy humans. Fasting glucose and insulin levels and the homeostasis model assessment of insulin resistance value showed that obesity was associated with insulin resistance. The skeletal muscle level of HSF1 was decreased in obese and ob/ob mice. HSF1 was selectively over-expressed in the skeletal muscles of high fat diet (HFD)-fed mice. Muscle HSF1 over-expression successfully triggered glycolytic-to-oxidative myofiber switch and increased fatty acid metabolism and insulin sensitivity in the skeletal muscles of HFD-fed mice. Moreover, HSF1 improved energy expenditure and blocked muscle accumulation of triglycerides in HFD-fed mice. Consequently, muscle HSF1 mitigated the impaired muscle insulin signaling and insulin resistance in HFD-fed mice. In conclusion, T2DM and obesity in HFD-fed mice may be treated with selective HSF1-directed programming of exercise-like effects in skeletal muscle. These findings may aid the development of a new therapeutic approach for obesity and T2DM.

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Section: Discussionsupporting

confidence: 52%

Skeletal muscle HSF1 prevents insulin resistance by improving glucose utilization

Lin

et al. 2022

The FASEB Journal

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“…The mRNA levels of hsf1 and sp1 showed identical in runx1 GFP + cells and in runx1 GFP − cells, and maintained stable in runx1 GFP + cells after Cu stresses ( Figure S10 E). However, SP1, MYC-SP1, or MYC-HSF1 ChIP-qPCR analyses showed that SP1 or HSF1 signals were less enriched at the promoter of FOXM1 in Cu-stressed group compared with the control ( Figures 8 C2-8C4), and Cu overload significantly up-regulated expression of HSF1 negative target BAX 44 , 45 while significantly down-regulated expressions of HSF1 positive target CDC6 and CKS1B 46 and SP1 positive targets CDC25A 47 and MYCA 48 ( Figure 8 D).…”

Section: Resultsmentioning

confidence: 96%

Copper overload impairs hematopoietic stem and progenitor cell proliferation via prompting HSF1/SP1 aggregation and the subsequently downregulating FOXM1-Cytoskeleton axis

Li¹,

Tai²,

Liu³

et al. 2023

iScience

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“…In breast cancer tissues, low levels of microRNA-615-5p correlated with high levels of HSF1 compared to normal tissues. Furthermore, microRNA-615-5p enhanced apoptosis and reduced the development of breast cancer by downregulating HSF1 expression [38]. These results suggest that increasing microRNA-615-5p, which is essential for tissue repair and blood vessel growth, could be a viable way to treat breast cancer.…”

Section: Breast Cancermentioning

confidence: 87%

“…In addition, HSF1 was identified as a predictive target gene of microRNA-615-5p, an angiogenesis and tissue repair gene [38]. In breast cancer tissues, low levels of microRNA-615-5p correlated with high levels of HSF1 compared to normal tissues.…”

Section: Breast Cancermentioning

confidence: 99%

Heat Shock Factor 1 Inhibition: A Novel Anti-Cancer Strategy with Promise for Precision Oncology

Gumilar,

Chin,

Ibrahim

et al. 2023

Cancers

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Heat shock factor 1 (HSF1) is a transcription factor crucial for regulating heat shock response (HSR), one of the significant cellular protective mechanisms. When cells are exposed to proteotoxic stress, HSF1 induces the expression of heat shock proteins (HSPs) to act as chaperones, correcting the protein-folding process and maintaining proteostasis. In addition to its role in HSR, HSF1 is overexpressed in multiple cancer cells, where its activation promotes malignancy and leads to poor prognosis. The mechanisms of HSF1-induced tumorigenesis are complex and involve diverse signaling pathways, dependent on cancer type. With its important roles in tumorigenesis and tumor progression, targeting HSF1 offers a novel cancer treatment strategy. In this article, we examine the basic function of HSF1 and its regulatory mechanisms, focus on the mechanisms involved in HSF1′s roles in different cancer types, and examine current HSF1 inhibitors as novel therapeutics to treat cancers.

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MicroRNA‑615‑5p regulates the proliferation and apoptosis of breast cancer cells by targeting HSF1

Cited by 10 publications

References 48 publications

Skeletal muscle HSF1 prevents insulin resistance by improving glucose utilization

Skeletal muscle HSF1 prevents insulin resistance by improving glucose utilization

Copper overload impairs hematopoietic stem and progenitor cell proliferation via prompting HSF1/SP1 aggregation and the subsequently downregulating FOXM1-Cytoskeleton axis

Heat Shock Factor 1 Inhibition: A Novel Anti-Cancer Strategy with Promise for Precision Oncology

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