Primary experimental results of methylseleninic acid on the proliferation inhibition and apoptotic induction in human high-metastatic large cell lung cancer cell line L9981

Jiewei Liu, Xiaorong Zhong, Qing Hua Zhou, Allen C Gao, Yanping Wang, Wen Zhu, Li Ma, Zhixuan Zhang

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Background and objective: It has been proved that selenium has remarkable effects in the prevention of cancer and proliferation inhibition for breast cancer and prostate cancer. Up to now, little is known, however, if methylseleninic acid (MSA) has the anticancer effect on lung cancer or not. The objective of this study is to detect the effect of MSA on proliferation inhibition and apoptotic induction for human high-metastatic large cell lung cancer cell line L9981, and to explore the molecular mechanisms. Methods: The changes of proliferation, clone formation, apoptotic level and cell cycles were detected in L9981 by trypan blue staining, clone formation suppression test, and flow cytometry before and after treating with different concentration of MSA. The expression level of proliferative-related and apoptotic-related genes was also determined in L9981 by flow cytometry. Results: (1) The proliferation ability of L9981 was remarkably inhibited at the concentration of 0.5 μmol/L of MSA (P<0. 05), and the cells were arrested at G0/G1 phase after treating with the same concentration. (2) Apoptosis of L9981 was remarkably induced by MSA at the concentration of 2.5 μmol/L (P<0. 05). (3) The clone formation ability of L9981 was significantly suppressed by MSA at the concentration of 5.0 μmol/L (P<0.05). (4) The expression levels of P53, P21, Fas, FasL and Bax were remarkably up-regulated after treatment with MSA. Conclusion: (1) MSA can significantly suppress the proliferation and clone formation ability of human high-metastatic large cell lung cancer cell line L9981, and also induce apoptosis of L9981. (2) The anticancer effects of MSA might be related to regulate the expression of cell cycle-related genes and apoptotic-related genes in the human high-metastatic large cell lung cancer line L9981.

Original languageEnglish (US)
Pages (from-to)103-108
Number of pages6
JournalChinese Journal of Lung Cancer
Volume9
Issue number2
StatePublished - Apr 20 2006
Externally publishedYes

Fingerprint

Lung Neoplasms
Cell Line
Clone Cells
Prostatic Neoplasms
Flow Cytometry
Apoptosis
methylselenic acid
cdc Genes
Cell Cycle Resting Phase
Trypan Blue
G1 Phase
Selenium
Genes
Cell Cycle
Staining and Labeling
Breast Neoplasms
Neoplasms

Keywords

  • Apoptosis
  • Growth inhibition
  • Human high-metastatic large cell lung cancer line L9981
  • Methylseleninic acid

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Cancer Research

Cite this

Primary experimental results of methylseleninic acid on the proliferation inhibition and apoptotic induction in human high-metastatic large cell lung cancer cell line L9981. / Liu, Jiewei; Zhong, Xiaorong; Zhou, Qing Hua; Gao, Allen C; Wang, Yanping; Zhu, Wen; Ma, Li; Zhang, Zhixuan.

In: Chinese Journal of Lung Cancer, Vol. 9, No. 2, 20.04.2006, p. 103-108.

Research output: Contribution to journalArticle

Liu, Jiewei ; Zhong, Xiaorong ; Zhou, Qing Hua ; Gao, Allen C ; Wang, Yanping ; Zhu, Wen ; Ma, Li ; Zhang, Zhixuan. / Primary experimental results of methylseleninic acid on the proliferation inhibition and apoptotic induction in human high-metastatic large cell lung cancer cell line L9981. In: Chinese Journal of Lung Cancer. 2006 ; Vol. 9, No. 2. pp. 103-108.
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abstract = "Background and objective: It has been proved that selenium has remarkable effects in the prevention of cancer and proliferation inhibition for breast cancer and prostate cancer. Up to now, little is known, however, if methylseleninic acid (MSA) has the anticancer effect on lung cancer or not. The objective of this study is to detect the effect of MSA on proliferation inhibition and apoptotic induction for human high-metastatic large cell lung cancer cell line L9981, and to explore the molecular mechanisms. Methods: The changes of proliferation, clone formation, apoptotic level and cell cycles were detected in L9981 by trypan blue staining, clone formation suppression test, and flow cytometry before and after treating with different concentration of MSA. The expression level of proliferative-related and apoptotic-related genes was also determined in L9981 by flow cytometry. Results: (1) The proliferation ability of L9981 was remarkably inhibited at the concentration of 0.5 μmol/L of MSA (P<0. 05), and the cells were arrested at G0/G1 phase after treating with the same concentration. (2) Apoptosis of L9981 was remarkably induced by MSA at the concentration of 2.5 μmol/L (P<0. 05). (3) The clone formation ability of L9981 was significantly suppressed by MSA at the concentration of 5.0 μmol/L (P<0.05). (4) The expression levels of P53, P21, Fas, FasL and Bax were remarkably up-regulated after treatment with MSA. Conclusion: (1) MSA can significantly suppress the proliferation and clone formation ability of human high-metastatic large cell lung cancer cell line L9981, and also induce apoptosis of L9981. (2) The anticancer effects of MSA might be related to regulate the expression of cell cycle-related genes and apoptotic-related genes in the human high-metastatic large cell lung cancer line L9981.",
keywords = "Apoptosis, Growth inhibition, Human high-metastatic large cell lung cancer line L9981, Methylseleninic acid",
author = "Jiewei Liu and Xiaorong Zhong and Zhou, {Qing Hua} and Gao, {Allen C} and Yanping Wang and Wen Zhu and Li Ma and Zhixuan Zhang",
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T1 - Primary experimental results of methylseleninic acid on the proliferation inhibition and apoptotic induction in human high-metastatic large cell lung cancer cell line L9981

AU - Liu, Jiewei

AU - Zhong, Xiaorong

AU - Zhou, Qing Hua

AU - Gao, Allen C

AU - Wang, Yanping

AU - Zhu, Wen

AU - Ma, Li

AU - Zhang, Zhixuan

PY - 2006/4/20

Y1 - 2006/4/20

N2 - Background and objective: It has been proved that selenium has remarkable effects in the prevention of cancer and proliferation inhibition for breast cancer and prostate cancer. Up to now, little is known, however, if methylseleninic acid (MSA) has the anticancer effect on lung cancer or not. The objective of this study is to detect the effect of MSA on proliferation inhibition and apoptotic induction for human high-metastatic large cell lung cancer cell line L9981, and to explore the molecular mechanisms. Methods: The changes of proliferation, clone formation, apoptotic level and cell cycles were detected in L9981 by trypan blue staining, clone formation suppression test, and flow cytometry before and after treating with different concentration of MSA. The expression level of proliferative-related and apoptotic-related genes was also determined in L9981 by flow cytometry. Results: (1) The proliferation ability of L9981 was remarkably inhibited at the concentration of 0.5 μmol/L of MSA (P<0. 05), and the cells were arrested at G0/G1 phase after treating with the same concentration. (2) Apoptosis of L9981 was remarkably induced by MSA at the concentration of 2.5 μmol/L (P<0. 05). (3) The clone formation ability of L9981 was significantly suppressed by MSA at the concentration of 5.0 μmol/L (P<0.05). (4) The expression levels of P53, P21, Fas, FasL and Bax were remarkably up-regulated after treatment with MSA. Conclusion: (1) MSA can significantly suppress the proliferation and clone formation ability of human high-metastatic large cell lung cancer cell line L9981, and also induce apoptosis of L9981. (2) The anticancer effects of MSA might be related to regulate the expression of cell cycle-related genes and apoptotic-related genes in the human high-metastatic large cell lung cancer line L9981.

AB - Background and objective: It has been proved that selenium has remarkable effects in the prevention of cancer and proliferation inhibition for breast cancer and prostate cancer. Up to now, little is known, however, if methylseleninic acid (MSA) has the anticancer effect on lung cancer or not. The objective of this study is to detect the effect of MSA on proliferation inhibition and apoptotic induction for human high-metastatic large cell lung cancer cell line L9981, and to explore the molecular mechanisms. Methods: The changes of proliferation, clone formation, apoptotic level and cell cycles were detected in L9981 by trypan blue staining, clone formation suppression test, and flow cytometry before and after treating with different concentration of MSA. The expression level of proliferative-related and apoptotic-related genes was also determined in L9981 by flow cytometry. Results: (1) The proliferation ability of L9981 was remarkably inhibited at the concentration of 0.5 μmol/L of MSA (P<0. 05), and the cells were arrested at G0/G1 phase after treating with the same concentration. (2) Apoptosis of L9981 was remarkably induced by MSA at the concentration of 2.5 μmol/L (P<0. 05). (3) The clone formation ability of L9981 was significantly suppressed by MSA at the concentration of 5.0 μmol/L (P<0.05). (4) The expression levels of P53, P21, Fas, FasL and Bax were remarkably up-regulated after treatment with MSA. Conclusion: (1) MSA can significantly suppress the proliferation and clone formation ability of human high-metastatic large cell lung cancer cell line L9981, and also induce apoptosis of L9981. (2) The anticancer effects of MSA might be related to regulate the expression of cell cycle-related genes and apoptotic-related genes in the human high-metastatic large cell lung cancer line L9981.

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KW - Growth inhibition

KW - Human high-metastatic large cell lung cancer line L9981

KW - Methylseleninic acid

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