MiR-92a Promotes Cell Metastasis of Colorectal Cancer Through PTEN-Mediated PI3K/AKT Pathway

Tao Wei Ke, Po Li Wei, Ken Tu Yeh, William Tzu Liang Chen, Ya Wen Cheng

Research output: Contribution to journalArticle

62 Citations (Scopus)

Abstract

Background: MicroRNAs regulate gene expression at the posttranscriptional level and play important roles in tumor development, progression, and metastasis. The aim of this study was to investigate the role of microRNA-92a (miR-92a) in metastasis of colorectal cancer (CRC). Methods: One hundred fifty-eight CRC patients were enrolled. The expression of miR-92a, PTEN, and E-cadherin was analyzed by real-time PCR. Univariate (Kaplan–Meier) analysis was used to analyze primary outcomes included 5-year overall survival and tumor recurrence. CRC cell model studies were used to analyze the miR-92a-involved CRC metastasis. Results: The expression of miR-92a in tumor tissues was significantly positively correlated with lymph node metastasis in CRC patients (p = 0.012). After adjusting for age, sex, and disease differentiation, this correlation remained significant (p = 0.01). In addition, there was a negative correlation between levels of miR-92a and the PTEN gene (p < 0.0001). No any association of miR-92a and E-cadherin was found (p = 0.128). Patients with high miR-92a/low PTEN had poorer overall survival and disease-free survival rates than those with high miR-92a/high PTEN, low miR-92a/high PTEN, and low miR-92a/low PTEN. The association of levels of miR-92a and PTEN with tumor cell migration in CRC was also confirmed in CRC cell models. Conclusions: We suggest that miR-92a is involved in lymph node metastasis of CRC patients through PTEN-regulated PI3K/AKT signaling pathway. © 2014, Society of Surgical Oncology.

Original languageEnglish
Pages (from-to)2649-2655
Number of pages7
JournalAnnals of Surgical Oncology
Volume22
Issue number8
DOIs
Publication statusPublished - Aug 1 2015

Fingerprint

MicroRNAs
Phosphatidylinositol 3-Kinases
Colorectal Neoplasms
Neoplasm Metastasis
Cadherins
Neoplasms
Lymph Nodes
Sex Differentiation
Survival
Disease-Free Survival
Cell Movement
Real-Time Polymerase Chain Reaction
Survival Rate
Gene Expression

ASJC Scopus subject areas

  • Surgery
  • Oncology

Cite this

MiR-92a Promotes Cell Metastasis of Colorectal Cancer Through PTEN-Mediated PI3K/AKT Pathway. / Ke, Tao Wei; Wei, Po Li; Yeh, Ken Tu; Chen, William Tzu Liang; Cheng, Ya Wen.

In: Annals of Surgical Oncology, Vol. 22, No. 8, 01.08.2015, p. 2649-2655.

Research output: Contribution to journalArticle

Ke, Tao Wei ; Wei, Po Li ; Yeh, Ken Tu ; Chen, William Tzu Liang ; Cheng, Ya Wen. / MiR-92a Promotes Cell Metastasis of Colorectal Cancer Through PTEN-Mediated PI3K/AKT Pathway. In: Annals of Surgical Oncology. 2015 ; Vol. 22, No. 8. pp. 2649-2655.
@article{9f4c65f42c2b42f5927d5b9a93fafcae,
title = "MiR-92a Promotes Cell Metastasis of Colorectal Cancer Through PTEN-Mediated PI3K/AKT Pathway",
abstract = "Background: MicroRNAs regulate gene expression at the posttranscriptional level and play important roles in tumor development, progression, and metastasis. The aim of this study was to investigate the role of microRNA-92a (miR-92a) in metastasis of colorectal cancer (CRC). Methods: One hundred fifty-eight CRC patients were enrolled. The expression of miR-92a, PTEN, and E-cadherin was analyzed by real-time PCR. Univariate (Kaplan–Meier) analysis was used to analyze primary outcomes included 5-year overall survival and tumor recurrence. CRC cell model studies were used to analyze the miR-92a-involved CRC metastasis. Results: The expression of miR-92a in tumor tissues was significantly positively correlated with lymph node metastasis in CRC patients (p = 0.012). After adjusting for age, sex, and disease differentiation, this correlation remained significant (p = 0.01). In addition, there was a negative correlation between levels of miR-92a and the PTEN gene (p < 0.0001). No any association of miR-92a and E-cadherin was found (p = 0.128). Patients with high miR-92a/low PTEN had poorer overall survival and disease-free survival rates than those with high miR-92a/high PTEN, low miR-92a/high PTEN, and low miR-92a/low PTEN. The association of levels of miR-92a and PTEN with tumor cell migration in CRC was also confirmed in CRC cell models. Conclusions: We suggest that miR-92a is involved in lymph node metastasis of CRC patients through PTEN-regulated PI3K/AKT signaling pathway. {\circledC} 2014, Society of Surgical Oncology.",
author = "Ke, {Tao Wei} and Wei, {Po Li} and Yeh, {Ken Tu} and Chen, {William Tzu Liang} and Cheng, {Ya Wen}",
year = "2015",
month = "8",
day = "1",
doi = "10.1245/s10434-014-4305-2",
language = "English",
volume = "22",
pages = "2649--2655",
journal = "Annals of Surgical Oncology",
issn = "1068-9265",
publisher = "Springer New York",
number = "8",

}

TY - JOUR

T1 - MiR-92a Promotes Cell Metastasis of Colorectal Cancer Through PTEN-Mediated PI3K/AKT Pathway

AU - Ke, Tao Wei

AU - Wei, Po Li

AU - Yeh, Ken Tu

AU - Chen, William Tzu Liang

AU - Cheng, Ya Wen

PY - 2015/8/1

Y1 - 2015/8/1

N2 - Background: MicroRNAs regulate gene expression at the posttranscriptional level and play important roles in tumor development, progression, and metastasis. The aim of this study was to investigate the role of microRNA-92a (miR-92a) in metastasis of colorectal cancer (CRC). Methods: One hundred fifty-eight CRC patients were enrolled. The expression of miR-92a, PTEN, and E-cadherin was analyzed by real-time PCR. Univariate (Kaplan–Meier) analysis was used to analyze primary outcomes included 5-year overall survival and tumor recurrence. CRC cell model studies were used to analyze the miR-92a-involved CRC metastasis. Results: The expression of miR-92a in tumor tissues was significantly positively correlated with lymph node metastasis in CRC patients (p = 0.012). After adjusting for age, sex, and disease differentiation, this correlation remained significant (p = 0.01). In addition, there was a negative correlation between levels of miR-92a and the PTEN gene (p < 0.0001). No any association of miR-92a and E-cadherin was found (p = 0.128). Patients with high miR-92a/low PTEN had poorer overall survival and disease-free survival rates than those with high miR-92a/high PTEN, low miR-92a/high PTEN, and low miR-92a/low PTEN. The association of levels of miR-92a and PTEN with tumor cell migration in CRC was also confirmed in CRC cell models. Conclusions: We suggest that miR-92a is involved in lymph node metastasis of CRC patients through PTEN-regulated PI3K/AKT signaling pathway. © 2014, Society of Surgical Oncology.

AB - Background: MicroRNAs regulate gene expression at the posttranscriptional level and play important roles in tumor development, progression, and metastasis. The aim of this study was to investigate the role of microRNA-92a (miR-92a) in metastasis of colorectal cancer (CRC). Methods: One hundred fifty-eight CRC patients were enrolled. The expression of miR-92a, PTEN, and E-cadherin was analyzed by real-time PCR. Univariate (Kaplan–Meier) analysis was used to analyze primary outcomes included 5-year overall survival and tumor recurrence. CRC cell model studies were used to analyze the miR-92a-involved CRC metastasis. Results: The expression of miR-92a in tumor tissues was significantly positively correlated with lymph node metastasis in CRC patients (p = 0.012). After adjusting for age, sex, and disease differentiation, this correlation remained significant (p = 0.01). In addition, there was a negative correlation between levels of miR-92a and the PTEN gene (p < 0.0001). No any association of miR-92a and E-cadherin was found (p = 0.128). Patients with high miR-92a/low PTEN had poorer overall survival and disease-free survival rates than those with high miR-92a/high PTEN, low miR-92a/high PTEN, and low miR-92a/low PTEN. The association of levels of miR-92a and PTEN with tumor cell migration in CRC was also confirmed in CRC cell models. Conclusions: We suggest that miR-92a is involved in lymph node metastasis of CRC patients through PTEN-regulated PI3K/AKT signaling pathway. © 2014, Society of Surgical Oncology.

UR - http://www.scopus.com/inward/record.url?scp=84938228202&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84938228202&partnerID=8YFLogxK

U2 - 10.1245/s10434-014-4305-2

DO - 10.1245/s10434-014-4305-2

M3 - Article

C2 - 25515201

AN - SCOPUS:84938228202

VL - 22

SP - 2649

EP - 2655

JO - Annals of Surgical Oncology

JF - Annals of Surgical Oncology

SN - 1068-9265

IS - 8

ER -