p53 functional activation is independent of its genotype in five esophageal squamous cell carcinoma cell lines

Ji, Junfang; Wu, Kun; Wu, Min; Zhan, Qimin

doi:10.1007/s11684-010-0260-x

Cited by 11 publications

(6 citation statements)

References 21 publications

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“…5b), indicating an inhibitory effect of p53 on AGPG expression. Furthermore, cells with WT TP53 (KYSE150) expressed much lower AGPG levels than those harboring mutant (MT) TP53 (TE-1 and KYSE30) 24 (Fig. 5c).…”

Section: Escc Gc Crcmentioning

confidence: 95%

Long noncoding RNA AGPG regulates PFKFB3-mediated tumor glycolytic reprogramming

et al. 2020

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Tumor cells often reprogram their metabolism for rapid proliferation. The roles of long noncoding RNAs (lncRNAs) in metabolism remodeling and the underlying mechanisms remain elusive. Through screening, we found that the lncRNA Actin Gamma 1 Pseudogene (AGPG) is required for increased glycolysis activity and cell proliferation in esophageal squamous cell carcinoma (ESCC). Mechanistically, AGPG binds to and stabilizes 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3). By preventing APC/C-mediated ubiquitination, AGPG protects PFKFB3 from proteasomal degradation, leading to the accumulation of PFKFB3 in cancer cells, which subsequently activates glycolytic flux and promotes cell cycle progression. AGPG is also a transcriptional target of p53; loss or mutation of TP53 triggers the marked upregulation of AGPG. Notably, inhibiting AGPG dramatically impaired tumor growth in patient-derived xenograft (PDX) models. Clinically, AGPG is highly expressed in many cancers, and high AGPG expression levels are correlated with poor prognosis, suggesting that AGPG is a potential biomarker and cancer therapeutic target.

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Section: Escc Gc Crcmentioning

confidence: 95%

Long noncoding RNA AGPG regulates PFKFB3-mediated tumor glycolytic reprogramming

et al. 2020

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“…Five-week-old male BALB/c nu/nu mice were purchased from the Institute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences. ESCC cell lines used in this study are listed in previous reports [ 14 - 15 , 88 - 90 ].…”

Section: Methodsmentioning

confidence: 99%

MiR-26a and miR-144 inhibit proliferation and metastasis of esophageal squamous cell cancer by inhibiting cyclooxygenase-2

et al. 2016

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The altered expression of miRNAs is involved in carcinogenesis of esophageal squamous cell carcinoma (ESCC), but whether miRNAs regulate COX-2 expression in ESCC is not clear. To this end, the expression levels of miR-26a and miR-144 in ESCC clinical tissues and cell lines were investigated by qRT-PCR. COX-2 and PEG2 were quantified by western blot and ELISA. Decrease in miR-26a and miR-144 expression in ESCC was found by a comparison between 30 pairs of ESCC tumor and adjacent normal tissues as well as in 11 ESCC cell lines (P < 0.001). Co-transfection of miR-26a and miR-144 in ESCC cell lines more significantly suppressed cell proliferation, migration, and invasion than did either miR-26a or miR-144 alone (all P < 0.001), as shown by assays of CCK8, migration and invasion and flow cytometry. The inhibitory effect of these two miRNAs in vivo was also verified in nude mice xenograft models. COX-2 was confirmed as a target of miR-26a and miR-144. In conclusion, miR-26a and miR-144 expression is downregulated in ESCC. Co-expression of miR-26a and miR-144 in ESCC cells resulted in inhibition of proliferation and metastasis in vitro and in vivo, suggesting that targeting COX-2 may be the mechanism of these two miRNAs.

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“…We further tested P53 protein level and found that P53 increased slightly in CRNN overexpressed cells compared with vector control cells. It was reported that p53 could be activated by DNA damage in KYSE30 with mutant p53 as other ESCC cell line with wide-type p53 [38]. qRT-PCR results also indicated that p21 mRNA level increased in CRNN overexpressed cells.…”

Section: Discussionmentioning

confidence: 87%

Characterization of Tumor Suppressive Function of cornulin in Esophageal Squamous Cell Carcinoma

Chen

Dai

et al. 2013

PLoS ONE

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By using cDNA microarray analysis, we identified cornulin (CRNN) gene was frequently downregulated in esophageal squamous cell carcinoma (ESCC). In the present study, we investigated the role of CRNN in ESCC development. The results showed that CRNN was frequently downregulated in primary ESCCs in both mRNA level (26/56, 46.4%) and protein level (137/249, 55%), which was significantly associated with lymph node metastases (P=0.027), advanced clinical stage (P=0.039), and overall survival rate (P<0.001). Multivariate analysis indicated that the CRNN downregulation was an independent prognostic factor for ESCC. Functional studies with both in vitro and in vivo assays demonstrated that CRNN had strong tumor suppressive ability in ESCC cells. The tumor-suppressive mechanism of CRNN was associated with its role in cell cycle arrest at G1/S checkpoint by upregulating expressions of P21WAF1/CIP1 and Rb. Silencing CRNN expression by RNA interference could effectively inhibit its tumor suppressive effect. In conclusion, our findings demonstrate that CRNN is a tumor suppressor gene that plays a critical tumor suppressive role in ESCC.

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p53 functional activation is independent of its genotype in five esophageal squamous cell carcinoma cell lines

Cited by 11 publications

References 21 publications

Long noncoding RNA AGPG regulates PFKFB3-mediated tumor glycolytic reprogramming

Long noncoding RNA AGPG regulates PFKFB3-mediated tumor glycolytic reprogramming

MiR-26a and miR-144 inhibit proliferation and metastasis of esophageal squamous cell cancer by inhibiting cyclooxygenase-2

Characterization of Tumor Suppressive Function of cornulin in Esophageal Squamous Cell Carcinoma

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