Trichostatin-A modulates claudin-1 mRNA stability through the modulation of Hu antigen R and tristetraprolin in colon cancer cells

Sharma, Ashok; Bhat, Ajaz A.; Krishnan, Moorthy; Singh, Amar B.; Dhawan, Punita

doi:10.1093/carcin/bgt207

Cited by 30 publications

(30 citation statements)

References 33 publications

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“…In this regard, studies in our lab using colon cancer cells found that in addition to the transcriptional regulation, claudin-1 expression is also regulated through the modulation of mRNA stability [72]. Our further analysis showed that histone deacetylase (HDAC)-dependent regulation of claudin-1 mRNA stability is mediated by the binding of Hu antigen R and Tristetraprolin to the 3 -UTR of claudin-1 mRNA [96]. Ribonomic and site-directed mutagenesis approaches were then used to confirm the binding of HuR and TTP to the 3 -UTR of claudin-1.…”

Section: Transcriptional and Post-transcriptional Regulationmentioning

confidence: 66%

Claudins and cancer: Fall of the soldiers entrusted to protect the gate and keep the barrier intact

Singh

Dhawan

2015

Seminars in Cell & Developmental Biology

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Section: Transcriptional and Post-transcriptional Regulationmentioning

confidence: 66%

Claudins and cancer: Fall of the soldiers entrusted to protect the gate and keep the barrier intact

Singh

Dhawan

2015

Seminars in Cell & Developmental Biology

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“…Previous studies showed that a few of drugs, including doxorubicin, vinblastine, etoposide, colchicine and daunorubicin, can promote ABCB1 gene expression in mammalian cells by enhancing its mRNA stability [23, 33]. In addition, a recent research found that TSA could modulate Claudin-1 mRNA stability in CRC cells [34]. Therefore, we speculated that HDACIs may regulate ABCB1 mRNA stability in CRC cells.…”

Section: Discussionmentioning

confidence: 96%

“…The particular mechanisms of ABCB1 mRNA stabilization in all of the above researches are unknown. The mRNA stability is tightly regulated by the interaction beteewn specific mRNA sequences and trans-acting factors, such as mRNA binding proteins and some microRNAs [6, 34]. Recently, mRNA binding proteins HuantigenR and Tristetraprolin have been reported play a crucial role in TSA-induced Claudin-1 mRNA stability [34].…”

Section: Discussionmentioning

confidence: 99%

“…The mRNA stability is tightly regulated by the interaction beteewn specific mRNA sequences and trans-acting factors, such as mRNA binding proteins and some microRNAs [6, 34]. Recently, mRNA binding proteins HuantigenR and Tristetraprolin have been reported play a crucial role in TSA-induced Claudin-1 mRNA stability [34]. Moreover, microRNAs have been implicated in the regulation of ABCB1 mRNA stability [35, 36].…”

Section: Discussionmentioning

confidence: 99%

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Histone deacetylase inhibitors regulate P-gp expression in colorectal cancer via transcriptional activation and mRNA stabilization

et al. 2016

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Histone deacetylase inhibitors (HDACIs) are emerging as a novel class of anti-tumor drugs. But the effect of HDACIs in tumors treatment has been disappointing, which mainly due to the acquisition of resistance to HDACIs. However, the underlying mechanisms have not been clearly understood. In this study, it was found that HDACIs SAHA and TSA increased P-gp expression in CRC cells, which has been well known to contribute to drug resistant. The mechanisms underlying these effects were investigated. We showed that HDACIs enhanced transcriptional activity of P-gp protein encoding gene ABCB1. HDACIs treatment also increased the protein and mRNA expression of STAT3, but not PXR, CAR, Foxo3a or β-catenin, which are known to be involved in ABCB transcription regulation. Interestingly, knockdown of STAT3 significantly attenuated HDACIs-induced P-gp up-regulation in colorectal cancer cells, suggesting that STAT3 plays a crucial role in HDACIs-up-regulated P-gp. Furthermore, this study revealed for the first time that HDACIs enhanced the stability of ABCB1 at post-transcriptional level. Taken together, these results proved that HDACIs induced P-gp expression by two distinct ways, transcriptional activation and mRNA stabilization. Our results suggested that more attention should be paid to the cancer treatment using HDACIs since they will induce multidrug resistance in cancer cells.

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“…Cdx2 can cooperate with Wnt pathway to regulate CLDN1 expression in colon cancer cells (29). The CLDN1 mRNA stability can also be regulated HDACdependently (31,32). To our knowledge, the immuno-profiles of CLDN1 and its association with β-catenin have not previously been reported in gastric cancer.…”

Section: Introductionmentioning

confidence: 85%

The expression of Claudin 1 correlates with β-catenin and is a prognostic factor of poor outcome in gastric cancer

Huang

et al. 2014

International Journal of Oncology

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Abstract. Claudin 1 is one of the tight junction proteins, which are critical in the maintenance of epithelial integrity. Aberrant regulation of CLDN1 and its correlation with β-catenin have been discovered in malignant tumors. The present study aimed to investigate the expression profile and clinical relevance of CLDN1 and β-catenin. The protein levels of CLDN1 and β-catenin were examined using immunohistochemical staining. The characteristics of expression profile and prognostic value were analyzed using Pearson's χ 2 test and Kaplan-Meier analysis, respectively. β-catenin overexpression and knockdown were used to investigate its role in regulating CLDN1 expression. We showed that CLDN1 was overexpressed in intestinal-type, presence of lymph node metastasis, higher TNM stage in gastric cancer patients and correlated with decreased overall survival. The characteristics of CLDN1 expression were associated with that of β-catenin. CLDN1 and β-catenin showed similar prognostic value in intestinal-type gastric cancers. β-catenin knockdown and overexpression in cell models revealed a positive relation between CLDN1 and β-catenin. Our study demonstrated that CLDN1 is a biomarker for intestinal-type gastric cancer with shorter survival. The expression of CLDN1 was strongly associated with β-catenin in gastric cancer patients and a gastric cancer cell model. IntroductionGastric cancer is the fourth most common cancer worldwide and is the second most common cause of cancer-related deaths.Gastric cancer has a poor prognosis (1). Although the 5-year survival rate in patients with early-stage disease is ~90%, since the vast majority present with distant metastasis, the overall 5-year survival rate is typically <20% (2). The 5-year survival rate has also been significantly correlated with the degree of tumor invasion, the presence of lymph node and/ or distant metastases and the TNM stage (3,4). However, very limited number of molecules that have clinicopathological significance in gastric cancer has been discovered.Claudin 1 (CLDN1) is one of the integral membrane proteins that constitute tight junctions. Tight junctions are essential for the tight sealing of cellular sheets and maintaining homeostasis (5). Absence of tight junctions or defective tight junctions is associated with the development of the neoplastic phenotype in epithelial cells (6). Thus it is accepted that the disruption of tight junctions leads to loss of cohesion, invasiveness and the lack of differentiation, thereby promoting tumorigenesis. CLDN1 is found to regulate intestinal epithelial homeostasis through the modulation of Notch-signaling (7). Many chemicals and nutrition can regulate CLDN1 expression through different pathways (8,9) to maintain the integrity of intestinal barrier function.The complexity of CLDN1 was proposed because its dual role as a tumor suppressor and promoter, as well as a positive and negative prognostic factor in different cancers, including breast (10,11), gastric (12), ovarian (13), lung (14) and colon (15-17). Decreased exp...

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Trichostatin-A modulates claudin-1 mRNA stability through the modulation of Hu antigen R and tristetraprolin in colon cancer cells

Cited by 30 publications

References 33 publications

Claudins and cancer: Fall of the soldiers entrusted to protect the gate and keep the barrier intact

Claudins and cancer: Fall of the soldiers entrusted to protect the gate and keep the barrier intact

Histone deacetylase inhibitors regulate P-gp expression in colorectal cancer via transcriptional activation and mRNA stabilization

The expression of Claudin 1 correlates with β-catenin and is a prognostic factor of poor outcome in gastric cancer

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