Epidermal growth factor-induced C/EBPbeta participates in EMT by dampening miR-203 in esophageal squamous cell carcinoma

Li, Junxia; Shan, Fabo; Xiong, Gang; Chen, Xuedan; Guan, Xingying; Wang, Ju Ming; Wang, Wen Lin; Xu, Xueqing; Bai, Yun

doi:10.1242/jcs.148759

Cited by 23 publications

(28 citation statements)

References 43 publications

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“…In this study, silencing of MEIS1 expression significantly suppressed the EGF expression in KYSE‐30 cells indicating that MEIS1 is involved in the EGF related signaling cascades. It is suggested that downregulation of EGF, as an epithelial factor, leads to decrease EMT (Li, Shan, et al, ). Taken together, our results illustrate that underexpression of TWIST1 and EGF , as two prevalent TFs of EMT promotion, can lead to a suppressed EMT in KYSE‐30 cells as an invasive cell line.…”

Section: Discussionmentioning

confidence: 99%

MEIS1 knockdown may promote differentiation of esophageal squamous carcinoma cell line KYSE‐30

Mahmoudian

Bahadori

Rad

et al. 2019

Molec Gen & Gen Med

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Background MEIS1 (Myeloid ecotropic viral integration site 1), as a homeobox (HOX) transcription factor, has a dual function in different types of cancer. Although numerous roles are proposed for MEIS1 in differentiation, stem cell function, gastrointestinal development and tumorigenesis, the involved molecular mechanisms are poor understood. Our aim in this study was to elucidate the functional correlation between MEIS1 , as regulator of differentiation process, and the involved genes in cell differentiation in human esophageal squamous carcinoma (ESC) cell line KYSE‐30. Methods The KYSE‐30 cells were transduced using recombinant retroviral particles containing specific shRNA sequence against MEIS1 to knockdown MEIS1 gene expression. Following RNA extraction and cDNA synthesis, mRNA expression of MEIS1 and the selected genes including TWIST1, EGF, CDX2, and KRT4 was examined using relative comparative real‐time PCR. Results Retroviral transduction caused a significant underexpression of MEIS1 in GFP‐hMEIS1 compared to control GFP cells approximately 5.5‐fold. While knockdown of MEIS1 expression caused a significant decrease in EGF and TWIST1 mRNA expression, nearly ‐8‐ and ‐12‐fold respectively, it caused a significant increase in mRNA expression of differentiation markers including KRT4 and CDX2 , approximately 34‐ and 1.14‐fold, correspondingly. Conclusion MEIS1 gene silencing in KYSE‐30 cells increased expression of epithelial markers and decreased expression of epithelial‐mesenchymal transition (EMT) marker TWIST1 . It may highlight the role of MEIS1 in differentiation process of KYSE‐30 cells. These results may confirm that MEIS1 silencing promotes differentiation and decreases EMT capability of ESC cell line KYSE‐30.

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Section: Discussionmentioning

confidence: 99%

MEIS1 knockdown may promote differentiation of esophageal squamous carcinoma cell line KYSE‐30

Mahmoudian

Bahadori

Rad

et al. 2019

Molec Gen & Gen Med

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“…Immunoreactive proteins were detected using SuperSignal West Dura Extended Duration Substrate (Thermo Scientific), after which the reactive bands were detected using enhanced chemiluminescence reagents (Thermo). To ensure the equal loading of samples in each lane, membranes were stripped and re-probed with an anti-β-actin antibody, as previously described [14]. …”

Section: Methodsmentioning

confidence: 99%

“…The expression levels of cyclin D1 and NF-κB-p65 were normalized to those of β-actin. The relative mRNA levels were calculated using the comparative threshold cycle method [14]. …”

Section: Methodsmentioning

confidence: 99%

Sphk1 promotes breast epithelial cell proliferation via NF-κB-p65-mediated cyclin D1 expression

Zhou

Zheng

et al. 2016

Oncotarget

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Lipid metabolism is crucially involved with the promotion of malignant progression and metastasis in various cancers. Growing evidence suggests that many types of cancers express high levels of sphingosine kinase 1 (Sphk1), which is known to mediate cell proliferation We hypothesized that Sphk1/sphingosine-1-phosphate (S1P) signaling contributes to tumor progression. In MCF10A and MCF10A-Sphk1 breast epithelial cells, we used TNF-α to activate the Sphk1/S1P pathway and the measured expression levels of NF-κBp65 and cyclin D1 mRNA and protein in the presence and absence of an NF-κB-p65 inhibitor. Chromatin immunoprecipitation assays were performed to determine whether NF-κB-p65 binds to the cyclin D1 promoter. We found that overexpression of Sphk1 induced NF-κB-p65 activation, increased expression of cyclin D1, shortened the cell division cycle, and thus promoted proliferation of breast epithelial cells. These findings provide insight into the mechanism by which an Sphk1/NF-κB-p65/cyclin D1 signaling pathway mediates cell proliferation.

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“…C/EBPβ downregulates AR in tumor cells and AR‐signaling in‐turn represses C/EBPβ expression . Furthermore, EGF receptor signaling stimulates C/EBPβ expression …”

Section: Introductionmentioning

confidence: 99%

Prostate cancer induces C/EBPβ expression in surrounding epithelial cells which relates to tumor aggressiveness and patient outcome

et al. 2018

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Background Implantation of rat prostate cancer cells into the normal rat prostate results in tumor‐stimulating adaptations in the tumor‐bearing organ. Similar changes are seen in prostate cancer patients and they are related to outcome. One gene previously found to be upregulated in the non‐malignant part of tumor‐bearing prostate lobe in rats was the transcription factor CCAAT/enhancer‐binding protein‐β (C/EBPβ). Methods To explore this further, we examined C/EBPβ expression by quantitative RT‐PCR, immunohistochemistry, and Western blot in normal rat prostate tissue surrounding slow‐growing non‐metastatic Dunning G, rapidly growing poorly metastatic (AT‐1), and rapidly growing highly metastatic (MatLyLu) rat prostate tumors―and also by immunohistochemistry in a tissue microarray (TMA) from prostate cancer patients managed by watchful waiting. Results In rats, C/EBPβ mRNA expression was upregulated in the surrounding tumor‐bearing prostate lobe. In tumors and in the surrounding non‐malignant prostate tissue, C/EBPβ was detected by immunohistochemistry in some epithelial cells and in infiltrating macrophages. The magnitude of glandular epithelial C/EBPβ expression in the tumor‐bearing prostates was associated with tumor size, distance to the tumor, and metastatic capacity. In prostate cancer patients, high expression of C/EBPβ in glandular epithelial cells in the surrounding tumor‐bearing tissue was associated with accumulation of M1 macrophages (iNOS+) and favorable outcome. High expression of C/EBPβ in tumor epithelial cells was associated with high Gleason score, high tumor cell proliferation, metastases, and poor outcome. Conclusions This study suggest that the expression of C/EBP‐beta, a transcription factor mediating multiple biological effects, is differentially expressed both in the benign parts of the tumor‐bearing prostate and in prostate tumors, and that alterations in this may be related to patient outcome.

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Epidermal growth factor-induced C/EBPbeta participates in EMT by dampening miR-203 in esophageal squamous cell carcinoma

Cited by 23 publications

References 43 publications

MEIS1 knockdown may promote differentiation of esophageal squamous carcinoma cell line KYSE‐30

MEIS1 knockdown may promote differentiation of esophageal squamous carcinoma cell line KYSE‐30

Sphk1 promotes breast epithelial cell proliferation via NF-κB-p65-mediated cyclin D1 expression

Prostate cancer induces C/EBPβ expression in surrounding epithelial cells which relates to tumor aggressiveness and patient outcome

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