Long noncoding RNA N-BLR upregulates the migration and invasion of gastric adenocarcinoma

Young Hoon Youn, Hyo Joo Byun, Jung Ho Yoon, Chan Hyuk Park, SangKil Lee

Research output: Contribution to journalArticle

Abstract

Background/Aims: Gastric cancer is one of the most common malignant tumors worldwide with poor prognosis due to a lack of effective treatment modalities. Recent research showed that a long noncoding RNA named N-BLR modulates the epithelial-to-mesenchymal transition (EMT) process in colorectal cancer. However, the biological role of N-BLR in gastric cancer still remains to be explored. The aim of this study was to investigate the possibility of N-BLR as an EMT modulator in gastric cancer. Methods: The expression of NBLR was measured by quantitative polymerase chain reaction in fresh gastric cancer tissue, paired adjacent normal tissues and cell lines. Fresh gastric tissues, paired samples obtained by surgery and clinical data were collected prospectively. Knockdown of N-BLR was induced by small interfering RNA (siRNAs). Cell number and viability were assessed after treatment with siRNAs. The ability of N-BLR to promote metastasis was measured using migration and invasion assays. Additionally, an inverse correlation between N-BLR and miR- 200c was measured by TaqMan microRNA assays. Western blotting was performed to detect EMT and apoptosis markers upon knockdown of N-BLR. Results: N-BLR expression was significantly elevated in gastric cancer cell lines and tissues compared to that in a normal gastric cell line and adjacent normal tissues (p<0.01). Two different siRNAs significantly reduced cell proliferation of gastric cancer cells compared to the siCT. siRNAs for N-BLR significantly suppressed migration and invasion in AGS and MKN28 cells. N-BLR expression was inversely correlated with miR-200c, which is known to regulate EMT. Conclusions: In this study, we confirmed NBLR as a regulator of the EMT process in gastric cancer.

Original languageEnglish
Pages (from-to)421-429
Number of pages9
JournalGut and liver
Volume13
Issue number4
DOIs
Publication statusPublished - 2019 Jan 1

Fingerprint

Long Noncoding RNA
Stomach Neoplasms
Epithelial-Mesenchymal Transition
Stomach
Adenocarcinoma
Up-Regulation
Small Interfering RNA
Cell Line
MicroRNAs
Colorectal Neoplasms
Cell Survival
Cell Count
Western Blotting
Cell Proliferation
Apoptosis
Neoplasm Metastasis
Polymerase Chain Reaction

All Science Journal Classification (ASJC) codes

  • Hepatology
  • Gastroenterology

Cite this

Youn, Young Hoon ; Byun, Hyo Joo ; Yoon, Jung Ho ; Park, Chan Hyuk ; Lee, SangKil. / Long noncoding RNA N-BLR upregulates the migration and invasion of gastric adenocarcinoma. In: Gut and liver. 2019 ; Vol. 13, No. 4. pp. 421-429.
@article{b2f523b89d2b42138dd3da54af854e07,
title = "Long noncoding RNA N-BLR upregulates the migration and invasion of gastric adenocarcinoma",
abstract = "Background/Aims: Gastric cancer is one of the most common malignant tumors worldwide with poor prognosis due to a lack of effective treatment modalities. Recent research showed that a long noncoding RNA named N-BLR modulates the epithelial-to-mesenchymal transition (EMT) process in colorectal cancer. However, the biological role of N-BLR in gastric cancer still remains to be explored. The aim of this study was to investigate the possibility of N-BLR as an EMT modulator in gastric cancer. Methods: The expression of NBLR was measured by quantitative polymerase chain reaction in fresh gastric cancer tissue, paired adjacent normal tissues and cell lines. Fresh gastric tissues, paired samples obtained by surgery and clinical data were collected prospectively. Knockdown of N-BLR was induced by small interfering RNA (siRNAs). Cell number and viability were assessed after treatment with siRNAs. The ability of N-BLR to promote metastasis was measured using migration and invasion assays. Additionally, an inverse correlation between N-BLR and miR- 200c was measured by TaqMan microRNA assays. Western blotting was performed to detect EMT and apoptosis markers upon knockdown of N-BLR. Results: N-BLR expression was significantly elevated in gastric cancer cell lines and tissues compared to that in a normal gastric cell line and adjacent normal tissues (p<0.01). Two different siRNAs significantly reduced cell proliferation of gastric cancer cells compared to the siCT. siRNAs for N-BLR significantly suppressed migration and invasion in AGS and MKN28 cells. N-BLR expression was inversely correlated with miR-200c, which is known to regulate EMT. Conclusions: In this study, we confirmed NBLR as a regulator of the EMT process in gastric cancer.",
author = "Youn, {Young Hoon} and Byun, {Hyo Joo} and Yoon, {Jung Ho} and Park, {Chan Hyuk} and SangKil Lee",
year = "2019",
month = "1",
day = "1",
doi = "10.5009/gnl18408",
language = "English",
volume = "13",
pages = "421--429",
journal = "Gut and Liver",
issn = "1976-2283",
publisher = "Joe Bok Chung",
number = "4",

}

Long noncoding RNA N-BLR upregulates the migration and invasion of gastric adenocarcinoma. / Youn, Young Hoon; Byun, Hyo Joo; Yoon, Jung Ho; Park, Chan Hyuk; Lee, SangKil.

In: Gut and liver, Vol. 13, No. 4, 01.01.2019, p. 421-429.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Long noncoding RNA N-BLR upregulates the migration and invasion of gastric adenocarcinoma

AU - Youn, Young Hoon

AU - Byun, Hyo Joo

AU - Yoon, Jung Ho

AU - Park, Chan Hyuk

AU - Lee, SangKil

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Background/Aims: Gastric cancer is one of the most common malignant tumors worldwide with poor prognosis due to a lack of effective treatment modalities. Recent research showed that a long noncoding RNA named N-BLR modulates the epithelial-to-mesenchymal transition (EMT) process in colorectal cancer. However, the biological role of N-BLR in gastric cancer still remains to be explored. The aim of this study was to investigate the possibility of N-BLR as an EMT modulator in gastric cancer. Methods: The expression of NBLR was measured by quantitative polymerase chain reaction in fresh gastric cancer tissue, paired adjacent normal tissues and cell lines. Fresh gastric tissues, paired samples obtained by surgery and clinical data were collected prospectively. Knockdown of N-BLR was induced by small interfering RNA (siRNAs). Cell number and viability were assessed after treatment with siRNAs. The ability of N-BLR to promote metastasis was measured using migration and invasion assays. Additionally, an inverse correlation between N-BLR and miR- 200c was measured by TaqMan microRNA assays. Western blotting was performed to detect EMT and apoptosis markers upon knockdown of N-BLR. Results: N-BLR expression was significantly elevated in gastric cancer cell lines and tissues compared to that in a normal gastric cell line and adjacent normal tissues (p<0.01). Two different siRNAs significantly reduced cell proliferation of gastric cancer cells compared to the siCT. siRNAs for N-BLR significantly suppressed migration and invasion in AGS and MKN28 cells. N-BLR expression was inversely correlated with miR-200c, which is known to regulate EMT. Conclusions: In this study, we confirmed NBLR as a regulator of the EMT process in gastric cancer.

AB - Background/Aims: Gastric cancer is one of the most common malignant tumors worldwide with poor prognosis due to a lack of effective treatment modalities. Recent research showed that a long noncoding RNA named N-BLR modulates the epithelial-to-mesenchymal transition (EMT) process in colorectal cancer. However, the biological role of N-BLR in gastric cancer still remains to be explored. The aim of this study was to investigate the possibility of N-BLR as an EMT modulator in gastric cancer. Methods: The expression of NBLR was measured by quantitative polymerase chain reaction in fresh gastric cancer tissue, paired adjacent normal tissues and cell lines. Fresh gastric tissues, paired samples obtained by surgery and clinical data were collected prospectively. Knockdown of N-BLR was induced by small interfering RNA (siRNAs). Cell number and viability were assessed after treatment with siRNAs. The ability of N-BLR to promote metastasis was measured using migration and invasion assays. Additionally, an inverse correlation between N-BLR and miR- 200c was measured by TaqMan microRNA assays. Western blotting was performed to detect EMT and apoptosis markers upon knockdown of N-BLR. Results: N-BLR expression was significantly elevated in gastric cancer cell lines and tissues compared to that in a normal gastric cell line and adjacent normal tissues (p<0.01). Two different siRNAs significantly reduced cell proliferation of gastric cancer cells compared to the siCT. siRNAs for N-BLR significantly suppressed migration and invasion in AGS and MKN28 cells. N-BLR expression was inversely correlated with miR-200c, which is known to regulate EMT. Conclusions: In this study, we confirmed NBLR as a regulator of the EMT process in gastric cancer.

UR - http://www.scopus.com/inward/record.url?scp=85069294609&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85069294609&partnerID=8YFLogxK

U2 - 10.5009/gnl18408

DO - 10.5009/gnl18408

M3 - Article

C2 - 30970439

AN - SCOPUS:85069294609

VL - 13

SP - 421

EP - 429

JO - Gut and Liver

JF - Gut and Liver

SN - 1976-2283

IS - 4

ER -