Retinoic acid inhibits pancreatic cancer cell migration and EMT through the downregulation of IL-6 in cancer associated fibroblast cells

Guan, Jian; Zhang, Hui; Zhang, Wen; Gu, Yumei; Cheng, Yin; Sun, Yang; Zhang, Tingting; Jia, Congwei; Lü, Zhaohui; Chen, Jie

doi:10.1016/j.canlet.2013.12.006

Cited by 108 publications

(76 citation statements)

References 36 publications

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“…Molecular studies had demonstrated that retinoids (vitamin A and its metabolites) could cause apoptosis in pancreatic cancer cells and thus suppress pancreatic cancer growth via activation of retinoic acid receptor-gamma, suggesting that vitamin A and its metabolites may play a protective role against pancreatic cancer22. Additionally, several preclinical studies showed that retinols play roles in many signaling pathways related with cell growth, adhesion and migration232425. A recent study revealed that retinoic acid could inhibit pancreatic cancer cell migration and epithelial-mesenchymal transition by decreasing the expression of interleukin 6 (IL-6) in cancer-associated fibroblast (CAFs) cells25, suggesting that retinoids could be applied for prevention or therapy the recurrence and metastasis of pancreatic cancer.…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, several preclinical studies showed that retinols play roles in many signaling pathways related with cell growth, adhesion and migration232425. A recent study revealed that retinoic acid could inhibit pancreatic cancer cell migration and epithelial-mesenchymal transition by decreasing the expression of interleukin 6 (IL-6) in cancer-associated fibroblast (CAFs) cells25, suggesting that retinoids could be applied for prevention or therapy the recurrence and metastasis of pancreatic cancer. Actually, immunotherapy including 13-cis-retinoic acid and interleukin 2 had been used for treating locally advanced pancreatic cancer26.…”

Section: Discussionmentioning

confidence: 99%

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Association between vitamin A, retinol and carotenoid intake and pancreatic cancer risk: Evidence from epidemiologic studies

Huang

Yuan-fu

Zhi

et al. 2016

Sci Rep

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Pancreatic cancer is a devastating disease with poor prognosis. The association between vitamin A, retinol and carotenoid intake and the risk of pancreatic cancer occurrence remains controversial, and therefore it is necessary to make a meta-analysis to clarify the association between vitamin A, retinol and carotenoid intake and pancreatic cancer risk. In the present study, PubMed and EMBASE databases were used to identify qualified studies. The association between dietary vitamin A, retinol and carotenoids was estimated by pooled odds ratios (ORs) and corresponding 95% confidence intervals (CIs). It was found that there was an inverse correlation between vitamin A, beta-carotene and lycopene intake and the risk of pancreatic cancer (for vitamin A, pooled OR = 0.85, 95%CI = 0.74–0.97, P = 0.015; for beta-carotene, pooled OR = 0.78, 95%CI = 0.66–0.92, P = 0.003; for lycopene, pooled OR = 0.84, 95%CI = 0.73–0.97, P = 0.020), which was more prominent in case-control study subgroup. In conclusion, dietary vitamin A, beta-carotene and lycopene might inversely correlate with pancreatic cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Association between vitamin A, retinol and carotenoid intake and pancreatic cancer risk: Evidence from epidemiologic studies

Huang

Yuan-fu

Zhi

et al. 2016

Sci Rep

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“…This strategy is less specific to CAFs, but the broader effects of this compound might have greater tumoricidal properties; however, the possibility of widespread toxicity is also a concern. ATRA is currently used to treat multiple cancers and, in addition to other activities, it inhibits FAP, αSMA, and TGFβR expression in CAFs, thereby reducing ECM and cytokine secretion 306,307 , and subsequently, cancer cell proliferation and invasion. ATRA reverses chemoresistance through multiple mechanisms, but is metabolized by CYP26, which reduces its effects in multiple myeloma 228,309 ; inhibition of CYP26 with R115866 reversed the bortezomib-resistant phenotype of multiple myeloma-derived cells in pre-clinical co-culture and xenograft models 228 .…”

Section: Tumour-stroma Targeting Strategiesmentioning

confidence: 99%

Targeting the tumour stroma to improve cancer therapy

2018

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Cancers are not merely composed of cancer cells alone and, instead, are complex ‘ecosystems’ comprising many different cell types and noncellular factors. The tumour stroma is a critical component of the tumour microenvironment, where it has crucial roles in tumour initiation, progression, and metastasis. Most anticancer therapies target cancer cells specifically, but the tumour stroma can promote resistance of cancer cells to such therapies, eventually resulting in fatal disease. Therefore, novel treatment strategies should combine anticancer and antistroma agents. Herein, we provide an overview of the advances in understanding the complex cancer cell–tumour stroma interactions, and discuss how this knowledge can result in more effective therapeutic strategies, which might ultimately improve patient outcomes.

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“…Co-culturing CAFs with melanoma cells induced IL-8 secretion by CAFs, and inhibition of IL-6 and IL-8 abrogated the invasion of melanoma spheroids [30]. Retinoic acid, a lipophilic molecule derived from vitamin A, is thought to exert therapeutic effects by decreasing the secretion of IL-6 by CAFs, thereby limiting pancreatic cancer cell migration and induction of EMT [31,32]. …”

Section: The Role Of Caf-secreted Factors In Cancer Cell Migration Anmentioning

confidence: 99%

Cancer-associated fibroblasts modulate growth factor signaling and extracellular matrix remodeling to regulate tumor metastasis

Erdogan

Webb

2017

Biochemical Society Transactions

401

317

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Cancer-associated fibroblasts (CAFs) are major components of the surrounding stroma of carcinomas that emerge in the tumor microenvironment as a result of signals derived from the cancer cells. Biochemical cross-talk between cancer cells and CAFs as well as mechanical remodeling of the stromal extracellular matrix (ECM) by CAFs are important contributors to tumor cell migration and invasion, which are critical for cancer progression from a primary tumor to metastatic disease. In this review, we discuss key paracrine signaling pathways between CAFs and cancer cells that promote cancer cell migration and invasion. In addition, we discuss physical changes that CAFs exert on the stromal ECM to facilitate migration and invasion of cancer cells.

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Retinoic acid inhibits pancreatic cancer cell migration and EMT through the downregulation of IL-6 in cancer associated fibroblast cells

Cited by 108 publications

References 36 publications

Association between vitamin A, retinol and carotenoid intake and pancreatic cancer risk: Evidence from epidemiologic studies

Association between vitamin A, retinol and carotenoid intake and pancreatic cancer risk: Evidence from epidemiologic studies

Targeting the tumour stroma to improve cancer therapy

Cancer-associated fibroblasts modulate growth factor signaling and extracellular matrix remodeling to regulate tumor metastasis

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