Role of retinoids in the prevention and treatment of colorectal cancer

Applegate, Catherine C.; Lane, Michelle A.

doi:10.4251/wjgo.v7.i10.184

Cited by 51 publications

(34 citation statements)

References 180 publications

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“…The reduced migration and invasion of cancer cell lines induced by retinoids correlate in animal models with decreased tumor growth and metastases (Tabata et al, 2009;Zhao et al, 2009;Benelli et al, 2010;Applegate and Lane, 2015;Waters et al, 2015;Williams et al, 2018). These effects together with other beneficial actions have motivated the use of retinoids for the treatment of several malignancies, including acute promyelocytic leukemia (Cicconi et al, 2018;Lengfelder et al, 2018), head and neck squamous cell carcinoma (Bhatia et al, 2017), and neuroblastoma (Cheung, 2015).…”

Section: Downloaded Frommentioning

confidence: 99%

All-Trans Retinoic Acid Inhibits Migration and Invasiveness of Rheumatoid Fibroblast-Like Synoviocytes

Mosquera

Rodríguez-Trillo

Blanco

et al. 2019

J Pharmacol Exp Ther

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Fibroblast-like synoviocytes (FLSs) are pivotal in inflammation and joint damage of rheumatoid arthritis (RA). They acquire an active and aggressive phenotype, displaying increased migration and invasiveness and contributing to perpetuate synovial inflammation and destruction of cartilage and bone. The main current therapies of RA are focused against inflammatory factors and immune cells; however, a significant percentage of patients do not successfully respond. Combined treatments with drugs that control inflammation and that reverse the pathogenic phenotype of FLS could improve the prognosis of these patients. An unexplored area includes the retinoic acid, the main biologic retinoid, which is a candidate drug for many diseases but has reached clinical use only for a few. Here, we explored the effect of all-trans retinoic acid (ATRA) on the aggressive phenotype of FLS from patients with RA. RA FLSs were treated with ATRA, tumor necrosis factor (TNF), or TNF1ATRA, and cell migration and invasion were analyzed. In addition, a microarray analysis of expression, followed by gene-set analysis and quantitative polymerase chain reaction validation, was performed. We showed that ATRA induced a notable decrease in FLS migration and invasion that was accompanied by complex changes in gene expression. At supraphysiological doses, many of these effects were overridden or reverted by the concomitant presence of TNF. In conclusion, these results have demonstrated the therapeutic potential of retinoic acid on RA FLS provided TNF could be counterbalanced, either with high ATRA doses or with TNF inhibitors.

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Section: Downloaded Frommentioning

confidence: 99%

All-Trans Retinoic Acid Inhibits Migration and Invasiveness of Rheumatoid Fibroblast-Like Synoviocytes

Mosquera

Rodríguez-Trillo

Blanco

et al. 2019

J Pharmacol Exp Ther

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“…Accumulative researches indicated that retinoids were associated with the prevention and amelioration of numerous chronic diseases and cancers [29–32]. Retinoids are currently used as chemotherapies against cancers of epithelial origin [33].…”

Section: Introductionmentioning

confidence: 99%

“…In our previous studies, we reported that AtRA inhibited the NO production in proinflammatory cytokines stimulated peripheral blood mononuclear cells (PBMC) and monocytes from IBD and Alzheimer disease patients [11, 39]. Furthermore, retinoids are known to affect signaling pathways frequently altered which result in the development and progression of CRC [32]. In this sense, understanding the pathway involved in cancer-related inflammation and targeting transcription factors such as NF- κ B has attracted our attention.…”

Section: Introductionmentioning

confidence: 99%

All-Trans Retinoic Acid Modulates TLR4/NF-κB Signaling Pathway Targeting TNF-αand Nitric Oxide Synthase 2 Expression in Colonic Mucosa during Ulcerative Colitis and Colitis Associated Cancer

Rafa

Benkhelifa

Ait-Younes

et al. 2017

Mediators of Inflammation

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Colitis associated cancer (CAC) is the colorectal cancer (CRC) subtype that is associated with bowel disease such as ulcerative colitis (UC). The data on role of NF-κB signaling in development and progression of CAC were derived from preclinical studies, whereas data from human are rare. The aim of this work was to study the contribution of NF-κB pathway during UC and CAC, as well as the immunomodulatory effect of all-trans retinoic acid (AtRA). We analyzed the expression of NOS2, TNF-α, TLR4, and NF-κB, in colonic mucosa. We also studied NO/TNF-α modulation by LPS in colonic mucosa pretreated with AtRA. A marked increase in TLR4, NF-κB, TNF-α, and NOS2 expression was reported in colonic mucosa. The relationship between LPS/TLR4 and TNF-α/NO production, as well as the role of NF-κB signaling, was confirmed by ex vivo experiments and the role of LPS/TLR4 in NOS2/TNF-α induction through NF-κB pathway was suggested. AtRA downregulates NOS2 and TNF-α expression. Collectively, our study indicates that AtRA modulates in situ LPS/TLR4/NF-κB signaling pathway targeting NOS2 and TNF-α expression. Therefore, we suggest that AtRA has a potential value in new strategies to improve the current therapy, as well as in the clinical prevention of CAC development and progression.

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“…Colon cancer, an aggressive malignancy causes substantial morbidity and mortality (1,2). The current treatment for patients with colon cancer relies on chemotherapy, despite its severe side-effects.…”

Section: Introductionmentioning

confidence: 99%

Anticancer effects of oridonin on colon cancer are mediated via BMP7/p38 MAPK/p53 signaling

Liu

et al. 2018

Int J Oncol

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Colon cancer is a prevalent malignancy affecting the gastrointestinal tract. Oridonin (ORI) is a promising chemotherapeutic drug used in the treatment of colon cancer. In this study, we examined the anticancer activity of ORI against colon cancer and elucidated the underlying molecular mechanisms. Cell counting kit-8, flow cytometric and western blot analyses were conducted to analyze the growth inhibitory effects of ORI on SW620 cells; we employed BMP7 and p53 recombinant adenovirus to detect the influence of ORI on the p38 MAPK signal pathway; PT-qPCR, cell immunofluorescence staining and western blot analysis were used to detect the expression of BMP7, p38 and p-p38, p53 and p-p53. A xenograft tumor model and histological evaluation were introduced to detect the effects of ORI and BMP7 in SW620 cells in vivo. ORI inhibited the proliferation of SW620 cells and induced apoptosis. ORI also increased the total and phosphorylated levels of p53. The overexpression of p53 was found to enhance the anti-proliferative effects of ORI on the SW620 cells, while the inhibition of p53 partially reversed these effects. ORI increased the expression of bone morphogenetic protein 7 (BMP7) in the SW620 cells. The overexpression of BMP7 also enhanced the antiproliferative effects of ORI on the SW620 cells and reduced the growth rate of tumors in mice. BMP7-induced immunosuppression markedly decreased the anti-proliferative effects of ORI. ORI was not found to exert any substantial effect on the phosphorylation levels of Smad1/5/8, although it increased the level of p-p38 significantly. The inhibition of p38 significantly attenuated the ORI-induced increase in the levels of p-p53. The overexpression of BMP7 enhanced the promoting effects of ORI on the p-p53 and p-p38 levels, while BMP7-induced immunosuppression reduced the effects of ORI on p-p38 and p-p53. On the whole, the findings of this study suggest that ORI may be a promising agent for use in the treatment of colon cancer, and the anticancer effects of ORI may be partially mediated through the BMP7/p38 MAPK/p53 signaling pathway.

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Role of retinoids in the prevention and treatment of colorectal cancer

Cited by 51 publications

References 180 publications

All-Trans Retinoic Acid Inhibits Migration and Invasiveness of Rheumatoid Fibroblast-Like Synoviocytes

All-Trans Retinoic Acid Inhibits Migration and Invasiveness of Rheumatoid Fibroblast-Like Synoviocytes

All-Trans Retinoic Acid Modulates TLR4/NF-κB Signaling Pathway Targeting TNF-αand Nitric Oxide Synthase 2 Expression in Colonic Mucosa during Ulcerative Colitis and Colitis Associated Cancer

Anticancer effects of oridonin on colon cancer are mediated via BMP7/p38 MAPK/p53 signaling

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