Abnormal expression of genes that regulate retinoid metabolism and signaling in non-small-cell lung cancer

Кузнецова, Е. С.; Zinovieva, Olga L.; Oparina, N. Yu.; Prokofjeva, M. M.; Spirin, Pavel; Favorskaya, I. A.; Zborovskaya, I. B.; Лисицын, Н. А.; Prassolov, Vladimir; Mashkova, T. D.

doi:10.1134/s0026893316020138

Cited by 12 publications

(14 citation statements)

References 53 publications

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“…The same authors also correlated the decreased expression of ADH1B and ADH1C with advanced stages of colorectal carcinomas, overall indicating that dysregulation of the ATRA biosynthesis can be responsible of the cancer progression [83]. Similarly, in a later research, a different expression of genes involved in the retinoid's metabolism was found between 44 NSCLC tumor tissues and paired normal tissues [84]. Indeed, the authors recorded a dramatic decrease in mRNA levels of genes involved in the retinol oxidation to retinal (ADH1B, ADH3, RDHL), and in the conversion of retinal to ATRA (RALDH1), with an increased expression of AKR1B10 that converts retinal to retinol, indicating that in the resistant lung tumor tissue all the pathways concur to decrease ATRA concentrations [84].…”

Section: Metabolic Enzymesmentioning

confidence: 77%

“…Moreover, as RARβ, also RARα was defined as tumor suppressor silenced by extensive cytosine methylation in the promoter responsible of RARα under-expression in MCF-7 cell line, and probably in the dysregulation of ATRA signaling [185]. In a lung cancer key research, a different expression of genes involved in the retinoid metabolism was found between 44 NSCLC tumor tissues and paired normal tissues [84]. The authors found that the mRNA levels of the nuclear receptor genes RXRγ, RARα, RXRα were significantly decreased in 80%, 65%, and 57% of tumor specimens, respectively, even at early stages.…”

Section: Other Rars and Rxrs Defectsmentioning

confidence: 99%

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Retinoic Acids in the Treatment of Most Lethal Solid Cancers

Costantini

Molinari

Farinon

et al. 2020

JCM

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Although the use of oral administration of pharmacological all-trans retinoic acid (ATRA) concentration in acute promyelocytic leukaemia (APL) patients was approved for over 20 years and used as standard therapy still to date, the same use in solid cancers is still controversial. In the present review the literature about the top five lethal solid cancers (lung, stomach, liver, breast, and colon cancer), as defined by The Global Cancer Observatory of World Health Organization, and retinoic acids (ATRA, 9-cis retinoic acid, and 13-cis retinoic acid, RA) was compared. The action of retinoic acids in inhibiting the cell proliferation was found in several cell pathways and compartments: from membrane and cytoplasmic signaling, to metabolic enzymes, to gene expression. However, in parallel in the most aggressive phenotypes several escape routes have evolved conferring retinoic acids-resistance. The comparison between different solid cancer types pointed out that for some cancer types several information are still lacking. Moreover, even though some pathways and escape routes are the same between the cancer types, sometimes they can differently respond to retinoic acid therapy, so that generalization cannot be made. Further studies on molecular pathways are needed to perform combinatorial trials that allow overcoming retinoic acids resistance.

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Section: Metabolic Enzymesmentioning

confidence: 77%

Section: Other Rars and Rxrs Defectsmentioning

confidence: 99%

Retinoic Acids in the Treatment of Most Lethal Solid Cancers

Costantini

Molinari

Farinon

et al. 2020

JCM

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“…As possible explanation, it has been reported that genes related to retinoid biosynthesis, transport, degradation and signaling are deregulated in most NSCLC [47], possibly explaining at least in part those contradictory results. In particular, retinol is transformed in retinal through many enzymes, all of which may be inactivated or non-functioning [47]. Finally, we showed that RARα expression was decreased and RARβ increased in CRBP-1 + where compared to empty-transfected H460 cells.…”

Section: Discussionmentioning

confidence: 99%

“…A greater and significant downregulation of pAKT, pERK and pEGFR in CRBP-1 + compared to empty-transfected H460 cells was documented after 48 h of 5 µM at RA treatment, but not after retinol treatment. As possible explanation, it has been reported that genes related to retinoid biosynthesis, transport, degradation and signaling are deregulated in most NSCLC [ 47 ], possibly explaining at least in part those contradictory results. In particular, retinol is transformed in retinal through many enzymes, all of which may be inactivated or non-functioning [ 47 ].…”

Section: Discussionmentioning

confidence: 99%

Cellular retinol binding protein 1 transfection reduces proliferation and AKT-related gene expression in H460 non-small lung cancer cells

et al. 2020

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In recent years, new treatments with novel action mechanisms have been explored for advanced non-small cell lung cancer (NSCLC). Retinoids promote cancer cell differentiation and death and their trafficking and action is mediated from specific cytoplasmic and nuclear receptors, respectively. The purpose of this study was to investigate the effect of Cellular retinol binding protein-1 (CRBP-1) transfection in H460 human NSCLC cell line, normally not expressing CRBP-1. H460 cells were transfected by using a vector pTargeT Mammalian expression system carrying the whole sequence of CRBP-1 gene. For proliferation and apoptosis studies, cells were treated with different concentrations of all-trans Retinoic Acid (atRA) and retinol. AKT-related gene expression was analyzed by using western blot and Signosis array and results analysed by one-way analysis of variance (ANOVA) or by t-student test. CRBP-1+ showed reduced proliferation and viability in basal condition and after atRA treatment when compared to empty-transfected H460 cells. Reduced proliferation in CRBP-1+ H460 cells associated to the down-regulation of pAKT/pERK/pEGFR-related genes. In particular, gene array documented the down-regulation of AKT and Stat-3-related genes, including M-Tor, Akt1, Akt2, Akt3, Foxo1, p27, Jun. Restoration of CRBP-1 expression in H460 cells reduced proliferation and viability in both basal condition and after atRA treatment, likely by down-regulating AKT-related gene level. Further studies are needed to better clarify how those CRBP-1-related intracellular pathways contribute to counteract NSCLC progression in order to suggest a potential tool to improve efficacy of retinoid anti lung cancer adjuvant therapy.

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“…5 13 Both SOX-2 and TTF-1(NK2X-1 ) genes are associated with tumour plasticity 14 and a decrease in expression of genes that regulate retinoid metabolism and signalling, including RALDH1, has also been reported in non-small cell lung cancers. 15 Although most cancers associated with type 1 CPAMs are mucinous adenocarcinomas 5 13 and therefore negative for TTF-1, persistence of SOX-2 expression and loss of RALDH1 in the epithelial cells may have some bearing on tumour development and warrant further study.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of lung development in the aetiology of adult congenital pulmonary airway malformations

Taylor

Rice

Nicholson

et al. 2020

Thorax

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Congenital pulmonary airway malformations (CPAMs) are rare lung abnormalities that result in cyst formation and are associated with respiratory distress in infants and malignant potential in adults. The pathogenesis of CPAMs remains unknown but data suggest disruption of the normal proximo-distal programme of airway branching and differentiation. Here, we demonstrate that adult human CPAM are lined with epithelium that retains SOX-2 and thyroid transcription factor-1 immunohistochemical markers, characteristic of the developing lung. However, RALDH-1, another key marker, is absent. This suggests a more complex aetiology for CPAM than complete focal arrest of lung development and may provide insight to the associated risk of malignancy.

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Abnormal expression of genes that regulate retinoid metabolism and signaling in non-small-cell lung cancer

Cited by 12 publications

References 53 publications

Retinoic Acids in the Treatment of Most Lethal Solid Cancers

Retinoic Acids in the Treatment of Most Lethal Solid Cancers

Cellular retinol binding protein 1 transfection reduces proliferation and AKT-related gene expression in H460 non-small lung cancer cells

Mechanism of lung development in the aetiology of adult congenital pulmonary airway malformations

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