Activated STAT3 may participate in tumor progression through increasing CD133/survivin expression in early stage of colon cancer

Wanlu Li, Mi Ra Lee, Taeyeong Kim, YoungWan Kim, Meeyon Cho

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

The activation of signal transducer and activator of transcription 3 (STAT3) by elevated interleukin (IL) levels has been reported to regulate tumorigenesis both in vitro and in vivo. However, the clinical implication of p-STAT3 expression in colon cancer is still controversial. In this study, we evaluated the effect of STAT3 inactivation on biologic behavior of primary (Caco-2) and metastatic colon cancer cells (LoVo and SNU407) and the relation of p-STAT3 expression with the invasion of colon tumor. In vitro study, the STAT3 inhibition by siRNA and stattic treatment significantly reduced colony formation and cell migration and decreased CD133 and survivin the expression compared with a control in all three cell lines. Furthermore, primary cancer cells exhibited a marked decrease in CD133 expression and increased apoptosis compared to metastatic cells after stattic treatment. The immunohistochemical assay using clinical samples of colonic tumors with various invasion depth showed that p-STAT3 expression was inversely associated with tumor invasion (p = 0.001, hazard ratio (HR) = 0.328, 95% confidence interval (95%CI): 0.170–0.632). In conclusion, p-STAT3 may participate in the progression of the early stage of colon cancer through the up-regulation of CD133, which in turn induces survivin expression. However, the regulatory mechanism of these molecules in tumor progression in vivo is need to be more verified.

Original languageEnglish
Pages (from-to)354-361
Number of pages8
JournalBiochemical and Biophysical Research Communications
Volume497
Issue number1
DOIs
Publication statusPublished - 2018 Feb 26

Fingerprint

STAT3 Transcription Factor
Colonic Neoplasms
Tumors
Neoplasms
Cells
Interleukins
Small Interfering RNA
Cell Movement
Assays
Hazards
Colon
Carcinogenesis
Up-Regulation
Chemical activation
Confidence Intervals
Apoptosis
Cell Line
Molecules

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

@article{957127fce16d4824ab479fc43615dd68,
title = "Activated STAT3 may participate in tumor progression through increasing CD133/survivin expression in early stage of colon cancer",
abstract = "The activation of signal transducer and activator of transcription 3 (STAT3) by elevated interleukin (IL) levels has been reported to regulate tumorigenesis both in vitro and in vivo. However, the clinical implication of p-STAT3 expression in colon cancer is still controversial. In this study, we evaluated the effect of STAT3 inactivation on biologic behavior of primary (Caco-2) and metastatic colon cancer cells (LoVo and SNU407) and the relation of p-STAT3 expression with the invasion of colon tumor. In vitro study, the STAT3 inhibition by siRNA and stattic treatment significantly reduced colony formation and cell migration and decreased CD133 and survivin the expression compared with a control in all three cell lines. Furthermore, primary cancer cells exhibited a marked decrease in CD133 expression and increased apoptosis compared to metastatic cells after stattic treatment. The immunohistochemical assay using clinical samples of colonic tumors with various invasion depth showed that p-STAT3 expression was inversely associated with tumor invasion (p = 0.001, hazard ratio (HR) = 0.328, 95{\%} confidence interval (95{\%}CI): 0.170–0.632). In conclusion, p-STAT3 may participate in the progression of the early stage of colon cancer through the up-regulation of CD133, which in turn induces survivin expression. However, the regulatory mechanism of these molecules in tumor progression in vivo is need to be more verified.",
author = "Wanlu Li and Lee, {Mi Ra} and Taeyeong Kim and YoungWan Kim and Meeyon Cho",
year = "2018",
month = "2",
day = "26",
doi = "10.1016/j.bbrc.2018.02.084",
language = "English",
volume = "497",
pages = "354--361",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Academic Press Inc.",
number = "1",

}

Activated STAT3 may participate in tumor progression through increasing CD133/survivin expression in early stage of colon cancer. / Li, Wanlu; Lee, Mi Ra; Kim, Taeyeong; Kim, YoungWan; Cho, Meeyon.

In: Biochemical and Biophysical Research Communications, Vol. 497, No. 1, 26.02.2018, p. 354-361.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Activated STAT3 may participate in tumor progression through increasing CD133/survivin expression in early stage of colon cancer

AU - Li, Wanlu

AU - Lee, Mi Ra

AU - Kim, Taeyeong

AU - Kim, YoungWan

AU - Cho, Meeyon

PY - 2018/2/26

Y1 - 2018/2/26

N2 - The activation of signal transducer and activator of transcription 3 (STAT3) by elevated interleukin (IL) levels has been reported to regulate tumorigenesis both in vitro and in vivo. However, the clinical implication of p-STAT3 expression in colon cancer is still controversial. In this study, we evaluated the effect of STAT3 inactivation on biologic behavior of primary (Caco-2) and metastatic colon cancer cells (LoVo and SNU407) and the relation of p-STAT3 expression with the invasion of colon tumor. In vitro study, the STAT3 inhibition by siRNA and stattic treatment significantly reduced colony formation and cell migration and decreased CD133 and survivin the expression compared with a control in all three cell lines. Furthermore, primary cancer cells exhibited a marked decrease in CD133 expression and increased apoptosis compared to metastatic cells after stattic treatment. The immunohistochemical assay using clinical samples of colonic tumors with various invasion depth showed that p-STAT3 expression was inversely associated with tumor invasion (p = 0.001, hazard ratio (HR) = 0.328, 95% confidence interval (95%CI): 0.170–0.632). In conclusion, p-STAT3 may participate in the progression of the early stage of colon cancer through the up-regulation of CD133, which in turn induces survivin expression. However, the regulatory mechanism of these molecules in tumor progression in vivo is need to be more verified.

AB - The activation of signal transducer and activator of transcription 3 (STAT3) by elevated interleukin (IL) levels has been reported to regulate tumorigenesis both in vitro and in vivo. However, the clinical implication of p-STAT3 expression in colon cancer is still controversial. In this study, we evaluated the effect of STAT3 inactivation on biologic behavior of primary (Caco-2) and metastatic colon cancer cells (LoVo and SNU407) and the relation of p-STAT3 expression with the invasion of colon tumor. In vitro study, the STAT3 inhibition by siRNA and stattic treatment significantly reduced colony formation and cell migration and decreased CD133 and survivin the expression compared with a control in all three cell lines. Furthermore, primary cancer cells exhibited a marked decrease in CD133 expression and increased apoptosis compared to metastatic cells after stattic treatment. The immunohistochemical assay using clinical samples of colonic tumors with various invasion depth showed that p-STAT3 expression was inversely associated with tumor invasion (p = 0.001, hazard ratio (HR) = 0.328, 95% confidence interval (95%CI): 0.170–0.632). In conclusion, p-STAT3 may participate in the progression of the early stage of colon cancer through the up-regulation of CD133, which in turn induces survivin expression. However, the regulatory mechanism of these molecules in tumor progression in vivo is need to be more verified.

UR - http://www.scopus.com/inward/record.url?scp=85042116244&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85042116244&partnerID=8YFLogxK

U2 - 10.1016/j.bbrc.2018.02.084

DO - 10.1016/j.bbrc.2018.02.084

M3 - Article

C2 - 29432737

AN - SCOPUS:85042116244

VL - 497

SP - 354

EP - 361

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 1

ER -