Publications by authors named "Cuifeng Xia"

4 Publications

  • Page 1 of 1

PirB functions as an intrinsic suppressor in hippocampal neural stem cells.

Aging (Albany NY) 2021 06 13;13(12):16062-16071. Epub 2021 Jun 13.

Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Kunming, Yunnan 650223, China.

Neural stem cells play pivotal roles during prenatal development and throughout life. Here, we report that Paired immunoglobulin-like receptor B (PirB) functions as a suppressor during brain neurogenesis in the adult mouse. PirB expression increased with age during development, and its deficiency promoted neural stem cell proliferation and differentiation and . Furthermore, we detected an increase in Type 1 neural stem cells in PirB-deficient mice compared to their wild-type littermates. PirB deficiency promoted stemness marker gene expression of Sox2 and KLF4 by activating Akt1 phosphorylation. These findings suggest that PirB inhibits the self-renewal and differentiation capacities of neural stem cells. Thus, PirB may have the potential to serve as a therapeutic target for treatment of reduced neurogenesis in adults due to aging or other pathological conditions.
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http://dx.doi.org/10.18632/aging.203134DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8266311PMC
June 2021

Circ_0026344 restrains metastasis of human colorectal cancer cells via miR-183.

Artif Cells Nanomed Biotechnol 2019 Dec;47(1):4038-4045

Department of Colorectal Surgery, The Third Affiliated Hospital of Kunming Medical University , Kunming , China.

CircRNA circ_0026344 was previously revealed as a tumour-suppressive gene in colorectal cancer (CRC) progression. The purpose of this research was to investigate the role of circ_0026344 in CRC cells metastasis induced by chemokines. Two human CRC cell lines SW480 and Caco-2 were treated by CCL20 and CXCL8. Cell proliferation, migration/invasion, expression of epithelial-mesenchymal transition (EMT) inducers and the expression of circ_0026344 were measured using sulforhodamine B assay, Transwell chamber, western blot and qRT-PCR, respectively. The effects of circ_0026344 on CRC cells migration/invasion and the expression of EMT inducers were evaluated. Moreover, the downstream miRNA and signalling pathways of circ_0026344 were studied. CCL20 and CXCL8 synergized to facilitate the proliferation, migration and invasion of CRC cells. At the meantime, E-cadherin was downregulated, whereas N-cadherin, Vimentin and Snail were up-regulated by CCL20 and CXCL8 co-stimulation, which was accompanied by the mobilization of PI3K/AKT/ERK signalling. More interestingly, the expression of circ_0026344 was down-regulated by CCL20 and CXCL8 co-stimulation. Silence of circ_0026344 increased the migratory and invasive capacities of CRC cells and increased EMT process as well. Overexpression of circ_0026344 led to a contrary impact. miR-183 was negatively regulated by circ_0026344, and the inhibitory effects of circ_0026344 overexpression on Wnt/β-catenin pathway were reversed when miR-183 was overexpressed. Overexpression of circ_0026344 restrained CRC metastasis and EMT induced by CCL20 and CXCL8 synergistical treatment. miR-183 was a downstream effector of circ_0026344, and the anti-tumour function of circ_0026344 might be involved in the repressed Wnt/β-catenin signalling. Highlights CCL20 and CXCL8 synergize to decrease the expression of circ_0026344; Silence of circ_0026344 promotes CRC cells migration, invasion and EMT process; miR-183 is a downstream effector of circ_0026344.
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http://dx.doi.org/10.1080/21691401.2019.1669620DOI Listing
December 2019

Erlotinib inhibits colon cancer metastasis through inactivation of TrkB-dependent ERK signaling pathway.

J Cell Biochem 2019 Feb 5. Epub 2019 Feb 5.

Department of Colorectal Surgery, The Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.

The distal metastasis is the main cause of death in patients with colon cancer. Tyrosine receptor kinase B (TrkB) and ERK signals may be the potential targets for the treatment of colon cancer metastasis. This study aims to investigate whether erlotinib inhibits distant metastasis of colon cancer by regulating TrkB and ERK signaling pathway. Human colon adenocarcinoma cell lines (SW480 and Caco-2) pretreated with exogenous C-X-C motif chemokine ligand 8 (CXCL8) were used to assess the suppressive effect of erlotinib on tumor metastasis, including anoikis, epithelial-mesenchymal transformation (EMT), migration, and invasion. Through TrkB overexpression, Akt suppression, and ERK suppression, the roles of TrkB, Akt, and ERK in erlotinib-induced metastasis inhibition of colon cancer cells were explored. The results showed that erlotinib alleviated CXCL8-induced metastasis of the colon cancer cells. Overexpression of TrkB in colon cancer cells eliminated the effect of erlotinib on anoikis, inhibition of EMT, migration, and invasion, and downregulation of p-ERK and p-Akt. Furthermore, the inhibition of ERK activation instead of Akt activation was found to participate in erlotinib-mediated metastasis resistance, including anoikis, inhibition of EMT, migration, and invasion. In conclusion, erlotinib inhibits colon cancer cell anoikis resistance, EMT, migration, and invasion by inactivating TrkB-dependent ERK signaling pathway.
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http://dx.doi.org/10.1002/jcb.28400DOI Listing
February 2019

CXCL8 induces epithelial-mesenchymal transition in colon cancer cells via the PI3K/Akt/NF-κB signaling pathway.

Oncol Rep 2017 Apr 14;37(4):2095-2100. Epub 2017 Feb 14.

Department of Colorectal Surgery, The Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650118, P.R. China.

The aim of the present study was to investigate the role of chemokine (C-X-C motif) ligand 8 (CXCL8) in the proliferation, invasiveness and metastasis of colon cancer and its role in the induction of epithelial-mesenchymal transition (EMT) via activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/nuclear factor-κB (NF-κB) pathway. The plasmid vector containing CXCL8 cDNA was transfected into LoVo cells using Lipofectamine 2000 reagent. Real-time PCR and western blot analyses were performed to determine expression of CXCL8. MTT growth inhibition, scratch and Transwell invasion assays were conducted to assess cell proliferation, migration and invasiveness of the CXCL8-transfected LoVo cells. Western blot analyses were conducted to measure the levels of phosphorylation of protein in the PI3K/Akt/NF-κB pathway in the CXCL8-transfected LoVo cells. Expression levels of CXCL8 mRNA and protein were significantly increased in the CXCL8-transfected LoVo cells compared with levels in the control and empty-vector cells (P<0.05). Overexpression of CXCL8 increased proliferation of the LoVo cells and significant differences in cell viability were observed 48 h after transfection (P<0.05) and remained significant at 72 and 96 h. CXCL8-transfected LoVo cells had a significantly higher migration rate and doubled invasion. The CXCL8-transfected LoVo cells exhibited an EMT-like phenotype, compared with control and empty-vector cells, with decreased expression of E-cadherin accompanied by increased expression of N-cadherin, vimentin and α-SMA. Overexpression of CXCL8 activated the PI3K/Akt/NF-κB pathway by promoting the phosphorylation of PI3K, Akt and NF-κB. Subcutaneous tumors were generated by subcutaneous injection of LoVo parental cells or CXCL8-transfected LoVo cells in BALB/c nude mice. The tumor growth was more rapid in the CXCL8-transfected group than that noted in the parental cell group. In conclusion, overexpression of CXCL8 induced cell proliferation, migration and invasion of colon cancer LoVo cells. CXCL8 may act through induction of EMT via the PI3K/AKT/NF-κB signaling axis.
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http://dx.doi.org/10.3892/or.2017.5453DOI Listing
April 2017
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