scholarly journals Tunicamycin aggravates cell migration, cell invasion and cell proliferation in colonic epithelial cells

2021 ◽  
Author(s):  
Rohit Gundamaraju ◽  
Ravichandra vemuri ◽  
Ranga Rao Ambati ◽  
Lakshminarayana Rangaswamy ◽  
Wenying Lu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Epithelial Cells ◽  
Cell Invasion ◽  
Gastrointestinal Cancers ◽  
Colonic Epithelial Cells ◽  
Positive Correlation ◽  
Preliminary Results ◽  
Clinical Conditions

Abstract Aim: Endoplasmic reticular stress (ERS) has been well-documented in escalating metastasis in clinical conditions. There has been a debate on its role in cancer portraying it as a double-edged sword. However, there is no evidence of increased cell migration and cell invasion under increased ERS by tunicamycin(TUN) 10μg/mL. Methods: In this study, we treated colonic epithelial cells (LS174T cells) with TUN and measured cell proliferation (by Ki67+ assay), cell migration and cell invasion at the 6th hour specifically. Results: Our results have demonstrated a positive correlation between TUN and cell migration, cell invasion, and proliferation. TUN treatment has significantly escalated cell invasion, migration and proliferation in LS174T cells. Conclusion: These preliminary results clearly suggest that TUN might promote metastasis of gastrointestinal cancers.

scholarly journals Hydroxyphenyl Butanone Induces Cell Cycle Arrest through Inhibition of GSK3β in Colorectal Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Songyan Zhang ◽  
Yunfeng Wang ◽  
Haopeng Zhang ◽  
Chengming Sun ◽  
Shuwei Dang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Epithelial Cells ◽  
Tumor Cells ◽  
Colony Formation ◽  
Colorectal Cancer Cell Line ◽  
Colonic Epithelial Cells ◽  
Low Concentration ◽  
Key Factor

Background. Colorectal cancer (CRC) is among the top three gastrointestinal malignancy in morbidity and mortality. The abnormal activation of Wnt/β-catenin pathway is considered to be a key factor in the occurrence and development of CRC. Novel inhibitor discovery against key factor in WNT pathway is important for CRC treatment and prevention. Methods. Cell proliferation was detected after hydroxyphenyl butanone treatment in human colorectal cancer HCT116, LOVO, and normal colonic epithelial NCM460 cells. Colony formation, cell invasion ability, and cell cycle were detected with and without GSK-3β knockdown. Results. Hydroxyphenyl butanone induces cycle arresting on G1-S phase of colorectal cancer cell line through GSK3β in Wnt/β-catenin pathway and inhibits malignant biological manifestations of cell proliferation, colony formation, and invasion. The inhibition in the high concentration group is stronger than that in the low concentration group, and the antitumor effect is different for different tumor cells. Under the same concentration of natural hydroxyphenyl butanone, the inhibition on normal colonic epithelial cells is significantly lower than that on tumor cells. The natural hydroxyphenyl butanone with medium and low concentration could promote the proliferation of normal colonic epithelial cells. Conclusion. This study illustrated natural hydroxyphenyl butanone as new inhibitor of GSK3β and revealed the mechanisms underlying the inhibitory effects in colorectal cancer.

scholarly journals PDGFRB knockdown rescues the efficacy of chemotherapy in metastatic gastric cancer patients

2021 ◽  
Author(s):  
Yang Tian ◽  
Wei Song ◽  
Shuping Yang ◽  
Zheng Chen ◽  
Ming Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Prognostic Factors ◽  
Cell Invasion ◽  
Cox Regression ◽  
Survival Curve ◽  
Metastatic Gastric Cancer ◽  
Akt Pathway

IntroductionThis study aimed to investigate the effect of PDGFRB on the efficacy of neoadjuvant chemotherapy (NAC) in metastatic gastric cancer (MGC).Material and methodsThe data from Gene Expression Omnibus (GEO) were analyzed to screen differentially expressed genes (DEGs). PDGFRB expression in cells were assessed by qRT-PCR and immunohistochemistry. Transwell, MTT and colony form assays were applied to determine the abilities of cell migration, cell invasion and cell proliferation. The association of core gene and PI3K/AKT pathway were identified through STRING database and western blot detection. Differences in overall survival (OS) among different patients were analyzed through Kaplan-Meier survival curve and prognostic factors were analyzed by Cox regression.ResultsHigh expression of PDGFRB and were found in gastric cancer through GEO data and MGC patients with combination chemotherapy resistance of docetaxel, cisplatin and S-1 (DCS therapy). Furthermore, the down-regulation of PDGFRB by PDGFRB shRNA or sunitinib malate could decrease cell migration, cell invasion and cell proliferation in resistant cells. Those findings were verified by in vivo experiments. Meanwhile, PDGFRB overexpression was accompany with the activation of PI3K/AKT pathway. In addition, the OS of patients in highly expressed PDGERB group were lower than that in lowly PDGFRB expressed group and PDGFRB, TNM staging and differentiation degree were the prognostic factors for MGC patients.ConclusionsPDGFRB knockdown could rescue the efficacy of chemotherapy in MGC and PDGFRB could serve as a novel marker for the prognosis of MGC.

TGF beta 1 promotes actin cytoskeleton reorganization and migratory phenotype in epithelial tracheal cells in primary culture

1996 ◽  
Vol 109 (9) ◽  
pp. 2207-2219 ◽  
Author(s):  
S. Boland ◽  
E. Boisvieux-Ulrich ◽  
O. Houcine ◽  
A. Baeza-Squiban ◽  
M. Pouchelet ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Epithelial Cells ◽  
Actin Cytoskeleton ◽  
Primary Culture ◽  
Tgf Beta ◽  
Cytoskeleton Reorganization ◽  
Extracellular Matrix Components ◽  
Migratory Phenotype

In the present study we have investigated the effects of transforming growth factor beta (TGF beta 1) on rabbit tracheal epithelial cells in primary culture, with respect to cell proliferation and differentiation. Epithelial tracheal cells derived from an explant plated on an extracellular matrix, formed an outgrowth resulting from cell division and cell migration. TGF beta 1 treatment produced a negative effect on cell proliferation, but in contrast, promoted a marked enhancement of cell migration and increase in outgrowth surface. TGF beta 1 induced marked cell shape changes, including cell spreading and lack of stratification, associated with reduced cell-cell contacts and increased cell-substratum anchorage, as seen by electron microscopic observations. Immunocytological studies demonstrated major TGF beta 1-induced actin cytoskeleton reorganization, corresponding to the development of a basal stress fiber network and decrease of the annular cell border, without affecting the tight junctions. The migratory phenotype was approached by microcinematography which clearly showed that TGF beta 1 triggered a stimulatory effect on migration of epithelial cells, determined using an image analyzing system. Present findings suggest a beneficial role for TGF beta 1 during wound healing in providing the acquisition of a migratory phenotype, with a higher capacity to migrate either on collagen or on different extracellular matrix components including laminin and fibronectin. Conversely, present data are not consistent with a squamous response to TGF beta 1, since metaplastic differentiation did not occur, as characterized by cytokeratin expression and cross-linked envelopes formation.

Interleukin-8 stimulates the migration of human colonic epithelial cells in vitro

1999 ◽  
Vol 97 (3) ◽  
pp. 385-390 ◽  
Author(s):  
Andrew J. WILSON ◽  
Keith BYRON ◽  
Peter R. GIBSON
Keyword(s):  
Cell Migration ◽  
Epithelial Cells ◽  
In Vitro Model ◽  
Interleukin 8 ◽  
Colonic Epithelium ◽  
Dependent Manner ◽  
Colonic Epithelial Cells ◽  
Tnf Α ◽  
Vitro Model

The migration of colonic epithelial cells (restitution) is an important event in the repair of mucosal injuries. Interleukin-8 (IL-8) is a physiological initiator of the chemotactic migration of leucocytes. This study aimed to determine whether IL-8 had a similar effect on migration in an in vitro model of wounded colonic epithelium. Cell migration over 24 h was assessed in circular wounds made in confluent monolayers of the human colon cancer cell line LIM1215. This migration was stimulated in a concentration-dependent manner by IL-8, with maximal effects of approx. 1.75-fold above basal migration. The motogenic effect of IL-8 was mediated independently of effects on cell proliferation. In contrast, it was partially dependent upon gene transcription and protein synthesis and involved the activation of pertussis-toxin-sensitive G-proteins. The short-chain fatty acids, acetate, propionate, butyrate and valerate, the activator of protein kinase C (phorbol-12-myristate-13-acetate) and tumour necrosis factor-α (TNF-α) all stimulated the secretion of IL-8. However, only the motogenic effect of TNF-α was dependent upon IL-8. In conclusion, IL-8 stimulated cell migration in an in vitro model of colonic epithelium, whereas the motogenic effect of at least one physiologically relevant factor was dependent upon an increase in its endogenous levels. If IL-8 stimulates colonic epithelial restitution in vivo, this would have ramifications for the control of repair processes following wounding of the colonic mucosa.

Hepatocyte growth factor promotes colonic epithelial regeneration via Akt signaling

2007 ◽  
Vol 293 (1) ◽  
pp. G230-G239 ◽  
Author(s):  
Masami Kanayama ◽  
Terumi Takahara ◽  
Yutaka Yata ◽  
Feng Xue ◽  
Eiji Shinno ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Akt Signaling ◽  
Colonic Epithelial Cells ◽  
Hepatocyte Growth

Hepatocyte growth factor (HGF) can promote the regeneration of injured organs, including HGF gene therapy by electroporation (EP) for liver injury. In this study, we investigated the effect of HGF on dextran sulfate sodium-induced colitis and tried to clarify the regenerative mechanisms of colonic epithelial cells and the signaling pathway involved. Colitis was induced by dextran sulfate sodium in mice, together with HGF gene transfer by EP. On day 10, the colitis was evaluated histologically and by Western blot analysis. The colonic epithelial cell line MCE301 was exposed to HGF protein, and its proliferation and activated signaling pathway were analyzed. In vivo, the histological score improved and the number of Ki-67-positive epithelial cells increased in the HGF-treated mice compared with the controls. Western blot analysis showed enhanced expression of phospho-Akt in the HGF-treated mice compared with the controls. In vitro, HGF stimulated the proliferation of MCE301 cells. There was enhanced phospho-Akt expression for more than 48 h after HGF stimulation, although phospho-ERK1/2 was enhanced for only 10 min. LY-294002 or Akt small interfering RNA suppressed cell proliferation induced by HGF. Thus HGF induces the proliferation of colonic epithelial cells via the phosphatidylinositol 3-kinase/Akt signaling pathway. HGF gene therapy can attenuate acute colitis via epithelial cell proliferation through the PI3K/Akt pathway. These data suggested that HGF gene therapy by EP may be effective for the regeneration and repair of injured epithelial cells in inflammatory bowel disease.

The chemokine KC regulates HGF-stimulated epithelial cell morphogenesis

2004 ◽  
Vol 286 (3) ◽  
pp. F581-F589 ◽  
Author(s):  
Joseph M. Ueland ◽  
Jane Gwira ◽  
Zhen-Xiang Liu ◽  
Lloyd G. Cantley
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Epithelial Cells ◽  
Collecting Duct ◽  
Neutrophil Migration ◽  
Branching Morphogenesis ◽  
Branch Points ◽  
Tubule Formation ◽  
Renal Epithelial Cells ◽  
Stimulation Of

Hepatocyte growth factor (HGF) induces migration, proliferation, and branching in renal epithelial cells from the inner medullary collecting duct (mIMCD-3 cells). Microarray analysis after HGF stimulation of these cells revealed upregulation of the chemokine KC. We found that both the message and protein levels of KC are increased after HGF treatment and that mIMCD-3 cells express the KC receptor CXCR2. Treatment with KC results in stimulation of mIMCD-3 cell proliferation but has no effect on basal rates of cell migration or branching morphogenesis. In contrast to its known stimulatory effect on neutrophil migration, KC markedly inhibits HGF-mediated cell migration and branching morphogenesis, resulting in shorter tubules with fewer branch points. Examination of the mechanism of this effect reveals that KC does not alter phosphorylation of the c-met receptor or the initial activation of the MAPK or phosphoinositide 3-kinase (PI 3-K) signaling pathways. However, sustained activation of the PI 3-K pathway by HGF was inhibited by treatment with KC, and mimicking this effect by treatment with LY-294002 2 h after HGF stimulation reproduced the inhibition of HGF-stimulated branching morphogenesis. These data demonstrate that HGF-mediated KC production can act in an autocrine fashion to downregulate excessive branching and migration of renal epithelial cells in response to HGF, while still supporting cell proliferation. These characteristics may play a role in modulating the response to HGF during developmental tubule formation and/or during the repair of the tubular architecture following injury.

scholarly journals lncRNA-ENST00000513396 is associated with multiple tumor signaling pathways, promotes the cell proliferation, invasion and migration in colorectal cancer

2021 ◽  
Author(s):  
Jinxin Zhu ◽  
Hui Wang ◽  
Yangbin Du ◽  
Zhenyu He
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Signaling Pathways ◽  
Cell Invasion ◽  
Tumor Cell Proliferation ◽  
Invasion And Migration ◽  
Multiple Tumor ◽  
And Migration ◽  
Cancer Tissues

Abstract Purpose Recently, many studies have revealed that Long noncoding RNAs (lncRNAs) were abundant in kinds of cells and might have multiple functions in a wide range of biological processes, such as proliferation, apoptosis, or cell migration. However, the role of lncRNA in the development of colorectal cancer has not been systematically reported and needs to be studied. Methods We applied Agilent microarray in tumoral tissues and paired para-cancer tissues for detecting different expression of lncRNAs and mRNAs. Bioinformatics analysis were used to identify the relationship between lncRNAs and corresponding mRNAs and the potential function of the lncRNAs. lncRNA-ENST00000430471 was chosen for further functional study through constructing overexpression plasmid, cell invasion, and cell migration. Results We found that 460 lncRNAs were significantly deregulated in cancer tissues. More importantly, they may participate in a variety of tumor-related signaling pathways through functional enrichment analysis with their co-expressed mRNAs, suggesting that these lncRNAs might play critical roles in tumorigenesis and development. Recently, we found lncRNA-ENST00000513396 was significantly upregulated in cancer tissues compared with para-cancer tissues. The overexpression of ENST00000513396 promotes tumor cell proliferation. Meanwhile ENST00000430471 could promote migration and invasion ability of colorectal cells. Conclusion LncRNAs play an important role in the development of colorectal cancer. Differentially expressed lncRNAs are associated with multiple tumor signaling pathways. Overexpression of lncRNA- ENST00000513396 in colorectal cancer cells can promote tumor cell proliferation and increase the ability of cell invasion and migration, which leads to the development of tumor.

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