Role of retinoic receptors in lung carcinogenesis

Bogos, Krisztina; Rényi-Vámos, F; Kovács, Gábor; Tóvári, József; Döme, Balázs

doi:10.1186/1756-9966-27-18

Cited by 27 publications

(19 citation statements)

References 50 publications

(51 reference statements)

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“…Retinoids regulate the growth and differentiation of normal, premalignant and malignant cell types, especially epithelial cells, mainly through interaction with nuclear retinoic acid receptors and retinoid X receptors (Bogos et al 2008). Vitamin A deficiency induces replacement of the normal pseudostratified mucociliary epithelium by a metaplastic stratified squamous epithelium in vivo.…”

Section: Resultsmentioning

confidence: 99%

Retinoic acid and hydrocortisone strengthen the barrier function of human RPMI 2650 cells, a model for nasal epithelial permeability

et al. 2012

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The nasal pathway represents an alternative route for non-invasive systemic administration of drugs. The main advantages of nasal drug delivery are the rapid onset of action, the avoidance of the first-pass metabolism in the liver and the easy applicability. In vitro cell culture systems offer an opportunity to model biological barriers. Our aim was to develop and characterize an in vitro model based on confluent layers of the human RPMI 2650 cell line. Retinoic acid, hydrocortisone and cyclic adenosine monophosphate, which influence cell attachment, growth and differentiation have been investigated on the barrier formation and function of the nasal epithelial cell layers. Real-time cell microelectronic sensing, a novel label-free technique was used for dynamic monitoring of cell growth and barrier properties of RPMI 2650 cells. Treatments enhanced the formation of adherens and tight intercellular junctions visualized by electron microscopy, the presence and localization of junctional proteins ZO-1 and b-catenin demonstrated by fluorescent immunohistochemistry, and the barrier function of nasal epithelial cell layers. The transepithelial resistance of the RPMI 2650 cell model reached 50 to 200 X 9 cm 2 , the permeability coefficient for 4.4 kDa FITC-dextran was 9.3 to 17 9 10 -6 cm/s, in agreement with values measured on nasal mucosa from in vivo and ex vivo experiments. Based on these results human RPMI 2650 cells seem to be a suitable nasal epithelial model to test different pharmaceutical excipients and various novel formulations, such as nanoparticles for toxicity and permeability.

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Section: Resultsmentioning

confidence: 99%

Retinoic acid and hydrocortisone strengthen the barrier function of human RPMI 2650 cells, a model for nasal epithelial permeability

et al. 2012

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“…Numerous retinoids have been developed, and their mechanisms of action are varied. (36) Four retinoids, ATRA, 13-cis-RA, 9-cis-RA, and 4-HPR, were used for our experiments. The combination of 100 lM EGCG with 10 lM ATRA, or 10 lM 13-cis-RA, or 10 lM 9-cis-RA, induced dramatically upregulated expression of the GADD153 gene in PC-9 cells 24 h after treatment (Table 1).…”

Section: Combination Of Egcg and Retinoidsmentioning

confidence: 99%

New cancer treatment strategy using combination of green tea catechins and anticancer drugs

Suganuma¹,

Saha²,

Fujiki³

2010

Cancer Science

161

107

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Green tea is now recognized as the most effective cancer preventive beverage. In one study, 10 Japanese-size cups of green tea daily supplemented with tablets of green tea extract limited the recurrence of colorectal polyps in humans to 50%. Thus, cancer patients who consume green tea and take anticancer drugs will have double prevention. We studied the effects of combining ())-epigallocatechin gallate (EGCG) and anticancer drugs, focusing on inhibition of cell growth and induction of apoptosis. Numerous anticancer drugs, such as tamoxifen, COX-2 inhibitors, and retinoids were used for the experiments, and the combination of EGCG and COX-2 inhibitors consistently induced the enhancement of apoptosis. To study the mechanism of the enhancement, we paid special attention to the enhanced expressions of DDIT3 (growth arrest and DNA damage-inducible 153, GADD153), GADD45A, and CDKN1A (p21 ⁄ WAF1 ⁄ CIP1) genes, based on our previous evidence that a combination of EGCG and sulindac specifically induced upregulated expression of GADD153 and p21 genes in PC-9 lung cancer cells. The synergistic enhancements of apoptosis and GADD153 gene expression in human non-small cell lung cancer cells by the combination of EGCG and celecoxib were mediated through the activation of the MAPK signaling pathway. This article reviews the synergistic enhancement of apoptosis, gene expression, and anticancer effects using various combinations of EGCG and anticancer drugs, including the combination of ())-epicatechin (EC) and curcumin. Based on the evidence, we present a new concept: green tea catechins as synergists with anticancer drugs. (Cancer Sci 2011; 102: 317-323) ''C ancer chemoprevention'' was defined in 1976,(1) and Michael Sporn (2) introduced the term ''combination cancer chemoprevention'' in the journal Nature in 1980. He defined the term as the combined use of several drugs with different mechanisms of action exerting marked synergistic preventive effects. In 1983, we began to study the cancer preventive activity of green tea catechins.(3,4) Green tea extract chemically contains at least four tea catechins: EGCG, ECG, EGC, and EC. The first three catechins induce cancer preventive activities, whereas EC is inactive.(5) We first reported that combinations with the active catechins and inactive EC induced synergistic effects on induction of apoptosis and inhibition of cell growth of human lung cancer cell line PC-9, and inhibition of TNF-a release from BALB ⁄ 3T3 cells treated with okadaic acid, a tumor promoter.(6) This suggests that whole green tea, which is a mixture of green tea catechins, is a more effective and practical cancer preventive than green tea catechins alone.(6) Using tritium ( 3 H)-EGCG we showed that EC induced the enhanced incorporation of 3 H-EGCG and other active green tea catechins into cells.(6) In addition, we recently showed that drinking 10 cups of green tea supplemented with green tea tablets significantly (50%) prevented recurrence of colorectal adenomas in patients who had received polypectomy 1 yea...

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“…It is well known that tRA is a differentiating agent used in the therapy of acute promyelocytic leukemia (APL) therapy, and it is under-used in other malignancies considering its low cost and low systemic toxicity [47][48][49]. In theory, tRA is an ideal candidate for cancer chemoprevention, as cancer is commonly characterized by abnormal growth with a lack of differentiation, which could be modified by tRA, and the combined applications of tRA with other drugs are also in clinical trials [50][51][52]. However, the knowledge of tRA inhibiting angiogenesis is rare, and this limits its usage in cancer therapy.…”

Section: Discussionmentioning

confidence: 99%

Targeting Angiogenesis by Blocking the ATM–SerRS–VEGFA Pathway for UV-Induced Skin Photodamage and Melanoma Growth

Song

Lü

Wang

et al. 2019

Cancers

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Retinoic acid (RA) has been widely used to protect skin from photo damage and skin carcinomas caused by solar ultraviolet (UV) irradiation, yet the mechanism remains elusive. Here, we report that all-trans retinoic acid (tRA) can directly induce the expression of a newly identified potent anti-angiogenic factor, seryl tRNA synthetase (SerRS), whose angiostatic role can, however, be inhibited by UV-activated ataxia telangiectasia mutated (ATM) kinase. In both a human epidermal cell line, HaCaT, and a mouse melanoma B16F10 cell line, we found that tRA could activate SerRS transcription through binding with the SerRS promoter. However, UV irradiation induced activation of ATM-phosphorylated SerRS, leading to the inactivation of SerRS as a transcriptional repressor of vascular endothelial growth factor A (VEGFA), which dampened the effect of tRA. When combined with ATM inhibitor KU-55933, tRA showed a greatly enhanced efficiency in inhibiting VEGFA expression and a much better protection of mouse skin from photo damage. Also, we found the combination greatly inhibited tumor angiogenesis and growth in mouse melanoma xenograft in vivo. Taken together, tRA combined with an ATM inhibitor can greatly enhance the anti-angiogenic activity of SerRS under UV irradiation and could be a better strategy in protecting skin from angiogenesis-associated skin damage and melanoma caused by UV radiation.

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Role of retinoic receptors in lung carcinogenesis

Cited by 27 publications

References 50 publications

Retinoic acid and hydrocortisone strengthen the barrier function of human RPMI 2650 cells, a model for nasal epithelial permeability

Retinoic acid and hydrocortisone strengthen the barrier function of human RPMI 2650 cells, a model for nasal epithelial permeability

New cancer treatment strategy using combination of green tea catechins and anticancer drugs

Targeting Angiogenesis by Blocking the ATM–SerRS–VEGFA Pathway for UV-Induced Skin Photodamage and Melanoma Growth

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