Estrogen receptor β potentiates the antiproliferative effect of raloxifene and affects the cell migration and invasion in HCT-116 colon cancer cells

Colon cancer is a common digestive system disease with an increasing incidence. Severe migration and invasion aggravates the deterioration of colon cancer patients. Previous studies have found that epithelial mesenchymal transition (EMT) is closely associated with early transference of colon carcinoma and abnormal changes occur in KIF18 signaling pathway. Butyrate protects colonic mucosa with a considerable effect on the colon. This study predicts that butyrate may reverse EMT process of colon cancer cells through KIF18 signaling pathway, thereby inhibiting cell migration and invasion. In this experiment, EMT model of colon cancer was used to investigate migration and invasion. Human colon cancer cell line SW1116 was cultured and assigned into control group (0 mmol/L butyrate), low concentration group (2 mmol/L), medium concentration group (4 mmol/L), and high concentration group (10 mmol/L). After 72 hours, cell migration and invasion was analyzed by Transwell assays. E-cadherin, Vimentin, and KIF18 level was detected by Western blot and quantitative real-time PCR. After treatment, cell migration and invasion was significantly inhibited compared to control dose-dependently. In addition, Vimentin and KIF18 mRNA level was significantly lower and E-cadherin mRNA was higher in treatment groups than control group in a dose-dependent manner (P < 0.05). Consistently, the profile of protein level of these molecules was similar to mRNA expression profile. Electron microscope showed that after treatment with butyrate, the surface protuberances of colon cancer cells were abnormally increased, especially the vesicular protuberances, which were the microvilli of intestinal mucosal epithelium. In conclusion, KIF18 is crucial in EMT of colon cancer cells. Butyrate may elevate E-cadherin and suppress Vimentin and KIF18 by activating KIF18 signaling, thus inhibiting invasion and migration.

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A role of zinc-finger protein 143 for cancer cell migration and invasion through ZEB1 and E-cadherin in colon cancer cells

Molecular Carcinogenesis ◽

10.1002/mc.22083 ◽

2013 ◽

Vol 53 (S1) ◽

pp. E161-E168 ◽

Cited By ~ 18

Author(s):

A Rome Paek ◽

Chang-Hoon Lee ◽

Hye Jin You

Keyword(s):

Colon Cancer ◽

Cell Migration ◽

Cancer Cells ◽

Zinc Finger ◽

Zinc Finger Protein ◽

Migration And Invasion ◽

Cancer Cell Migration ◽

Colon Cancer Cells ◽

Finger Protein

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Atypical role of sprouty in colorectal cancer: sprouty repression inhibits epithelial–mesenchymal transition

Oncogene ◽

10.1038/onc.2015.365 ◽

2015 ◽

Vol 35 (24) ◽

pp. 3151-3162 ◽

Cited By ~ 16

Author(s):

Q Zhang ◽

T Wei ◽

K Shim ◽

K Wright ◽

K Xu ◽

...

Keyword(s):

Colorectal Cancer ◽

Colon Cancer ◽

Cell Migration ◽

Cancer Cells ◽

Epithelial Mesenchymal Transition ◽

Migration And Invasion ◽

Colon Cancer Cells ◽

Mesenchymal Transition ◽

E Cadherin

Abstract Sprouty (SPRY) appears to act as a tumor suppressor in cancer, whereas we demonstrated that SPRY2 functions as a putative oncogene in colorectal cancer (CRC) (Oncogene, 2010, 29: 5241–5253). We investigated the mechanisms by which SPRY regulates epithelial–mesenchymal transition (EMT) in CRC. SPRY1 and SPRY2 mRNA transcripts were significantly upregulated in human CRC. Suppression of SPRY2 repressed AKT2 and EMT-inducing transcription factors and significantly increased E-cadherin expression. Concurrent downregulation of SPRY1 and SPRY2 also increased E-cadherin and suppressed mesenchymal markers in colon cancer cells. An inverse expression pattern between AKT2 and E-cadherin was established in a human CRC tissue microarray. SPRY2 negatively regulated miR-194-5p that interacts with AKT2 3′ untranslated region. Mir-194 mimics increased E-cadherin expression and suppressed cancer cell migration and invasion. By confocal microscopy, we demonstrated redistribution of E-cadherin to plasma membrane in colon cancer cells transfected with miR-194. Spry1 −/− and Spry2 −/− double mutant mouse embryonic fibroblasts exhibited decreased cell migration while acquiring several epithelial markers. In CRC, SPRY drive EMT and may serve as a biomarker of poor prognosis.

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Functional Estrogen Receptor β in Colon Cancer Cells

Biochemical and Biophysical Research Communications ◽

10.1006/bbrc.1999.1062 ◽

1999 ◽

Vol 261 (2) ◽

pp. 521-527 ◽

Cited By ~ 66

Author(s):

Gianna Fiorelli ◽

Lucia Picariello ◽

Valentina Martineti ◽

Francesco Tonelli ◽

Maria Luisa Brandi

Keyword(s):

Colon Cancer ◽

Estrogen Receptor ◽

Cancer Cells ◽

Estrogen Receptor Β ◽

Colon Cancer Cells

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Estrogen Receptor β mRNA in Colon Cancer Cells: Growth Effects of Estrogen and Genistein

Biochemical and Biophysical Research Communications ◽

10.1006/bbrc.2000.2444 ◽

2000 ◽

Vol 270 (2) ◽

pp. 425-431 ◽

Cited By ~ 88

Author(s):

Naoya Arai ◽

Anders Ström ◽

Joseph J. Rafter ◽

Jan-Åke Gustafsson

Keyword(s):

Colon Cancer ◽

Estrogen Receptor ◽

Cancer Cells ◽

Estrogen Receptor Β ◽

Colon Cancer Cells ◽

Growth Effects

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ID: 1029 Effects of carnosine on regulation of migration and invasion in human colorectal cancer cells

Biomedical Research and Therapy ◽

10.15419/bmrat.v4is.305 ◽

2017 ◽

Vol 4 (S) ◽

pp. 104 ◽

Cited By ~ 1

Author(s):

Po-Yu Lai ◽

Shu-Chen Hsieh ◽

Chih-Chung Wu ◽

Shu-Ling Hsieh

Keyword(s):

Colorectal Cancer ◽

Colon Cancer ◽

Cancer Cells ◽

Human Colon ◽

Migration And Invasion ◽

Colon Cancer Cells ◽

Human Colon Cancer ◽

Hct 116 ◽

Hct 116 Cells ◽

Human Colon Cancer Cells

Colorectal cancer is the third most commonly diagnosed cancer in the word. Carnosine is an endogenous dipeptide found in vertebrate skeletal muscles. It is known to have anti-fatigue, antioxidative, antihypertensive, antidiabetic, and cancer inhibiting effects. However, little research has been done regarding its influence on the metastasis of colon cancer. This study cultivated HCT-116 human colon cancer cells as a test model in order to investigate the impact of carnosine on the migration and invasion of human colon cancer cells. The results showed that 48-hour treatments of HCT-116 cells with 0.5, 1, or 5 mM carnosine each significantly inhibited the migration ability of the cells (P < 0.05). The 48-hour treatments with 0.5, 1, or 5 mM carnosine were also found to significantly reduce MMP-9 activity (P < 0.05), but not MMP-2 expression. Furthermore, when HCT-116 cells treated with 1 or 5 mM carnosine, invasion ability are significantly decreased and significantly increased E-cadherin expression (P < 0.05). On the other hand, the protein of TIMP-1, an inhibitor of MMP-9, is signification increased after 1 or 5 mM carnosine treatment (P<0.05). In addition, the u-PA protein level are significantly decreased after carnosine treatment. The results indicate that carnosine can regulate the migration and invasion by regulating MMPs and its regulator molecular expression in HCT-116 cells.

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Epigallocatechin-3-gallate inhibits proliferation and triggers apoptosis in colon cancer via the hedgehog/phosphoinositide 3-kinase pathways

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2020-0588 ◽

2021 ◽

Author(s):

Feng Ding ◽

Su Yang

Keyword(s):

Colon Cancer ◽

Tumor Growth ◽

Cancer Cells ◽

Nude Mice ◽

The Body ◽

Antiproliferative Effect ◽

Migration And Invasion ◽

Dependent Manner ◽

Colon Cancer Cells ◽

Underlying Mechanisms

The present study evaluated whether EGCG effectively attenuates tumor growth in colon cancer cells and in the xenografts of nude mice and to investigated the underlying mechanisms by focusing on the Shh and PI3K pathways. Three kinds of colon cancer cells and BALB/c nude mice were used to evaluate the antiproliferative effect of EGCG.The results showed that EGCG exhibited an antiproliferative effect against colon cancer cells in a dose-dependent manner with low toxicity against normal colon epithelial cells. Administration of EGCG caused significant apoptosis and inhibited the migration and invasion of colon cancer cells. The toxic effect of EGCG was accompanied by downregulation of the Shh and PI3K/Akt pathways. In addition, EGCG reduced tumor weight without affecting the body weight of nude mice and inhibited the activation of the Shh and PI3K/Akt pathways in tumor tissue. Purmorphamine (Shh agonist) or IGF-1 (PI3K agonist) partly abolished the effect of EGCG on cell proliferation, migration and apoptosis. Cyclopamine (Shh inhibitor) and LY294002 (PI3K inhibitor) showed the similar toxic effects as EGCG on colon cancer cells. In conclusion, EGCG inhibited colon tumor growth via downregulation of the Shh and PI3K pathways and may be a potential chemotherapeutic agent against colon cancer.

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