Retinoids in Lung Cancer: Friend, Foe, or Fellow Traveler?

Khuri, Fadlo R.; Lotan, Reuben

doi:10.1200/jco.2004.05.947

Cited by 13 publications

(6 citation statements)

References 26 publications

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“…This apoptosis may be inhibited by retinoic acid if RARβ is expressed on a normal level [ 43 ]. These findings explain in part the previous observation that RARβ expression is associated with poor prognosis among patients who are active smokers [ 44 ].…”

Section: Introductionsupporting

confidence: 75%

Role of retinoic receptors in lung carcinogenesis

Bogos

Rényi-Vámos

Kovács

et al. 2008

J Exp Clin Cancer Res

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Several in vitro and in vivo studies have examined the positive and negative effects of retinoids (vitamin A analogs) in premalignant and malignant lesions. Retinoids have been used as chemopreventive and anticancer agents because of their pleiotropic regulator function in cell differentiation, growth, proliferation and apoptosis through interaction with two types of nuclear receptors: retinoic acid receptors and retinoid X receptors. Recent investigations have gradually elucidated the function of retinoids and their signaling pathways and may explain the failure of earlier chemopreventive studies.In this review we have compiled basic and recent knowledge regarding the role of retinoid receptors in lung carcinogenesis. Sensitive and appropriate biological tools are necessary for screening the risk population and monitoring the efficacy of chemoprevention. Investigation of retinoid receptors is important and may contribute to the establishment of new strategies in chemoprevention for high-risk patients and in the treatment of lung cancer.

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Section: Introductionsupporting

confidence: 75%

Role of retinoic receptors in lung carcinogenesis

Bogos

Rényi-Vámos

Kovács

et al. 2008

J Exp Clin Cancer Res

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“…The other eight pathways in LUSC were retinol metabolism, drug metabolism cytochrome P450, xenobiotics, biological oxidations, androgen and estrogen biosynthesis and metabolism, Atrovastatin/Lovastatin/Simvastatin pathway, pharmacokinetics, and metabolism of xenobiotics by cytochrome P450. Retinoid might be associated with LUSC, but this needs further confirmation [28]. Cytochrome P450 was associated with cancer development, and polymorphisms are lung cancer risk factors [29].…”

Section: Discussionmentioning

confidence: 99%

LncRNAs are altered in lung squamous cell carcinoma and lung adenocarcinoma

2016

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Long non-coding RNAs (lncRNAs) have been implicated in pathogenesis of various cancers, including lung squamous cell carcinoma (LUSC) and lung adenocarcinoma (LUAD). We used cBioPortal to analyze lncRNA alteration frequencies and their ability to predict overall survival (OS) using 504 LUSC and 522 LUAD samples from The Cancer Genome Atlas (TCGA) database. In LUSC, 624 lncRNAs had alteration rates > 1% and 64 > 10%. In LUAD 625 lncRNAs had alteration rates > 1% and 36 > 10%. Among those, 620 lncRNAs had alteration frequencies > 1% in both LUSC and LUAD, while 22 were LUSC-specific and 23 were LUAD-specific. Twenty lncRNAs had alteration frequencies > 10% in both LUSC and LUAD, while 44 were LUSC-specific and 16 were LUAD specific. Genome ontology and pathway analyses produced similar results for LUSC and LUAD. Two lncRNAs (IGF2BP2-AS1 and DGCR5) correlated with better OS in LUSC, and three (MIR31HG, CDKN2A-AS1 and LINC01600) predicted poor OS in LUAD. Chip-seq and luciferase reporter assays identified potential IGF2BP2-AS1, DGCR5 and LINC01600 promoters and enhancers. This study presented lncRNA landscapes and revealed differentially expressed, highly altered lncRNAs in LUSC and LUAD. LncRNAs that act as oncogenes and lncRNA-regulating transcription factors provide novel targets for anti-lung cancer therapeutics.

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“…The exciting observations reported in the present study suggest that AKR1B10 inhibits the cellular differentiation produced by retinoic acid. It may also provide an explanation as to why clinical chemoprevention trials by h-carotenes and retinoids fail (21). h-Carotene for example is absorbed in the intestine and by the action of dioxygenase is a source of all-trans-retinal and 13-cis-retinal.…”

Section: Akr1b10 and Retinoic Acid Signalingmentioning

confidence: 99%

“…A recent study showed that decreased expression of retinoic acid receptors and retinoid X receptors was a frequent event in NSCLC; thus, a coordinated loss of retinoic acid signaling could be occurring in this disease (23). Moreover, retinoic acid receptor-h may be proapoptotic and an inhibitor of carcinogenesis in the former smoker but it may act as an inhibitor of apoptosis and enhancer of carcinogenesis in individuals that continue to smoke (21). Nonetheless, the observations reported in the present study will not only drive improvements in early diagnosis but provide an impetus to understand more about the roles of AKR1B10 and retinoids in lung cancer progression.…”

Section: Present Study and Future Directionsmentioning

confidence: 99%

AKR1B10: A New Diagnostic Marker of Non–Small Cell Lung Carcinoma in Smokers

Penning

2005

Clinical Cancer Research

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Retinoids in Lung Cancer: Friend, Foe, or Fellow Traveler?

Cited by 13 publications

References 26 publications

Role of retinoic receptors in lung carcinogenesis

Role of retinoic receptors in lung carcinogenesis

LncRNAs are altered in lung squamous cell carcinoma and lung adenocarcinoma

AKR1B10: A New Diagnostic Marker of Non–Small Cell Lung Carcinoma in Smokers

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