2016
DOI: 10.18632/aging.100987
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Abstract: Senescent cancer-associated fibroblasts (CAF) develop a senescence-associated secretory phenotype (SASP) that is believed to contribute to cancer progression. The mechanisms underlying SASP development are, however, poorly understood. Here we examined the functional role of microRNA in the development of the SASP in normal fibroblasts and CAF. We identified a microRNA, miR-335, up-regulated in the senescent normal fibroblasts and CAF and able to modulate the secretion of SASP factors and induce cancer cell mot… Show more

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Cited by 55 publications
(48 citation statements)
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References 43 publications
(53 reference statements)
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“…Higher levels of miR-335 lowered the abundance of phosphatase and tensin homologue (PTEN), in turn causing a rise in SASP factors like MMP2 and IL6 [55]. Senescent cells showed increased secretion of the protein cyclooxygenase 2 (PTGS2/COX2) and the signaling lipid prostaglandin E2 (PGE2).…”
Section: Micrornasmentioning
confidence: 99%
See 1 more Smart Citation
“…Higher levels of miR-335 lowered the abundance of phosphatase and tensin homologue (PTEN), in turn causing a rise in SASP factors like MMP2 and IL6 [55]. Senescent cells showed increased secretion of the protein cyclooxygenase 2 (PTGS2/COX2) and the signaling lipid prostaglandin E2 (PGE2).…”
Section: Micrornasmentioning
confidence: 99%
“…Senescent cells showed increased secretion of the protein cyclooxygenase 2 (PTGS2/COX2) and the signaling lipid prostaglandin E2 (PGE2). The levels of miR-335 were downregulated by inhibition of PTSG2/COX2 using celecoxib, which restored PTEN expression and decreased SASP [55]. …”
Section: Micrornasmentioning
confidence: 99%
“…One of the ways in which this COX-2 upregulation may lead to eventual loss of MTSS1 expression is through inflammation-mediated proteasome upregulation. Interleukin-6 (IL-6) is a known COX-2 dependent cytokine that exerts its effects through activation of oncogenic signaling pathways involved STAT3 [58, 59]. It has been shown that IL-6 upregulation can lead to increase in proteasome expression [60, 61].…”
Section: Discussionmentioning
confidence: 99%
“…And rapamycin, a clinically approved drug, inhibit cancer by targeting stromal fibroblasts. 40,41 Meanwhile a study found that NAC inhibits mTOR. 42 And the results in our study demonstrated that oxidative stress induced by colorectal cancer cells could stimulate autophagy in CAFs, which then led to intensive glycolysis and attenuated aerobic oxidation.…”
Section: Ccd-18-co Cell Viability (%)mentioning
confidence: 99%