Expression of PCNA and CD44mRNA in colorectal cancer with venous invasion and its relationship to liver metastasis

Yue, Shu-Qiang

doi:10.3748/wjg.v9.i12.2863

Cited by 19 publications

(14 citation statements)

References 42 publications

(16 reference statements)

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“…Mechanistically, our results show that HMGB1 induces CAC tumorigenesis and PCNA expression through the ERK1/2 signaling pathway. PCNA is a chief proliferation marker that reflects the level of cell proliferation [ 32 , 33 ]. Our finding is consistent with a previous report showing that blocking the RAGE-HMGB1 axis suppresses the growth and metastases of C6 glioma cells by inhibiting activation of the MAPK pathway [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

HMGB1 released from GSDME-mediated pyroptotic epithelial cells participates in the tumorigenesis of colitis-associated colorectal cancer through the ERK1/2 pathway

et al. 2020

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Background Pyroptosis is a form of proinflammatory gasdermin-mediated programmed cell death. Abnormal mucosal inflammation in the intestine is a critical risk factor for colitis-associated colorectal cancer (CAC). However, it is unknown whether pyroptosis participates in the development of CAC. Methods To investigate the role of gasdermin E (GSDME)-mediated pyroptosis in the development of CAC, Gsdme−/− mice and their wild-type (WT) littermate controls were challenged with azoxymethane (AOM) and dextran sodium sulfate (DSS) to induce a CAC model. Neutralizing antibodies against high-mobility group box protein 1 (HMGB1) were used to determine the role of HMGB1 in CAC. To identify the role of ERK1/2 in HMGB1-induced colon cancer cell proliferation, we performed western blotting and CCK8 assays using the ERK1/2-specific inhibitor U0126 in CT26 colon cancer cells. Results In the CAC model, Gsdme−/− mice exhibited reduced weight loss and colon shortening, attenuated rectal prolapse, and reduced tumor numbers and sizes compared to WT littermates. Furthermore, treatment with neutralizing anti-HMGB1 antibodies decreased the numbers and sizes of tumors, ERK1/2 activation and proliferating cell nuclear antigen (PCNA) expression in AOM/DSS-challenged WT mice. In addition, our in vitro experiments demonstrated that HMGB1 induced proliferation and PCNA expression in CT26 colon cancer cells through the ERK1/2 pathway. Conclusion GSDME-mediated pyroptosis promotes the development of CAC by releasing HMGB1, which induces tumor cell proliferation and PCNA expression through the ERK1/2 pathway. This finding reveals a previously unrecognized link between pyroptosis and CAC tumorigenesis and offers new insight into CAC pathogenesis.

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Section: Discussionmentioning

confidence: 99%

HMGB1 released from GSDME-mediated pyroptotic epithelial cells participates in the tumorigenesis of colitis-associated colorectal cancer through the ERK1/2 pathway

et al. 2020

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“…PCRs involved an initial denaturation at 94°C for 2 minutes and 30 seconds, followed by 25 or 40 cycles at 94°C for 30 seconds, and an appropriate annealing temperature (58°C to 65°C) for 30 seconds and then 72°C for 55 seconds. PCR primer sequences of the examined genes are shown in Table 2 33‐37 . The exponential phases of RT‐PCR amplification runs were determined from 25 to 40 cycles to allow quantitative comparisons among the cDNAs.…”

Section: Methodsmentioning

confidence: 99%

Cyclosporin‐Induced Downregulation of the Expression of E‐Cadherin During Proliferation of Edentulous Gingival Epithelium in Rats

Tu¹,

Chen²,

Shieh³

et al. 2006

Journal of Periodontology

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“…The DNA polymerase cofactor, proliferating cell nuclear antigen (20p12), regulates both synthesis of DNA and cell cycle, and expression of proliferating cell nuclear antigen has been found to associate with liver metastasis of CRC. 51 Adenosylhomocysteinase ( at 20q11) is required for Myc-induced mRNA cap methylation, protein synthesis and cell proliferation. 52,53 In 20q13.12, the transcription factor HNF4A manipulating polarity of epithelial cell showed facilitation in mouse intestine neoplasia.…”

Section: Frequent Copy Number Gains In Chromosome 20mentioning

confidence: 99%

Somatic gene copy number alterations in colorectal cancer: new quest for cancer drivers and biomarkers

et al. 2015

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Colorectal cancer (CRC) results from the accumulation of genetic alterations, and somatic copy number alterations (CNAs) are crucial for the development of CRC. Genome-wide survey of CNAs provides opportunities for identifying cancer driver genes in an unbiased manner. The detection of aberrant CNAs may provide novel markers for the early diagnosis and personalized treatment of CRC. A major challenge in array-based profiling of CNAs is to distinguish the alterations that play causative roles from the random alterations that accumulate during colorectal carcinogenesis. In this view, we systematically discuss the frequent CNAs in CRC, focusing on functional genes that have potential diagnostic, prognostic and therapeutic significance.

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Expression of PCNA and CD44mRNA in colorectal cancer with venous invasion and its relationship to liver metastasis

Cited by 19 publications

References 42 publications

HMGB1 released from GSDME-mediated pyroptotic epithelial cells participates in the tumorigenesis of colitis-associated colorectal cancer through the ERK1/2 pathway

HMGB1 released from GSDME-mediated pyroptotic epithelial cells participates in the tumorigenesis of colitis-associated colorectal cancer through the ERK1/2 pathway

Cyclosporin‐Induced Downregulation of the Expression of E‐Cadherin During Proliferation of Edentulous Gingival Epithelium in Rats

Somatic gene copy number alterations in colorectal cancer: new quest for cancer drivers and biomarkers

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