Effect of silencing TEM8 gene on proliferation, apoptosis, migration and invasion of XWLC‑05 lung cancer cells

Gong,Quan; Liu,Chao; Wang,Cunde; Zhuang,Li; Zhang,Lijuan; Wang,Xicai

doi:10.3892/mmr.2017.7959

Effect of silencing TEM8 gene on proliferation, apoptosis, migration and invasion of XWLC‑05 lung cancer cells

Authors:
- Quan Gong
- Chao Liu
- Cunde Wang
- Li Zhuang
- Lijuan Zhang
- Xicai Wang
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Affiliations: Department of Palliative Medicine, Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650118, P.R. China, Department of Nuclear Medicine, Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650118, P.R. China, Tumor Research Institute, Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650118, P.R. China
Published online on: November 3, 2017 https://doi.org/10.3892/mmr.2017.7959
Pages: 911-917
Copyright: © Gong et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Currently, the role of tumor endothelial marker 8 (TEM8) in the occurrence, development, invasion and metastasis of lung cancer and its mechanism are poorly understood. The present study aimed to investigate the effects of TEM8 on proliferation, apoptosis, migration and invasion of XWLC‑05 lung cancer cells. The expression of TEM8 in human lung cancer and adjacent tissues was detected by reverse transcription‑quantitative polymerase chain reaction and western blotting. An interference vector coding a short hairpin RNA (shRNA) targeting TEM8 was designed and transfected into XWLC‑05 lung cancer cells. MTT assay was used to detect cell proliferation. Flow cytometry was employed to detect cell cycle and apoptosis. Cell scratch assay was used for cell migration detection. Cell invasion ability was detected by the Transwell method. The expression of TEM8 in lung cancer tissues was significantly increased compared with adjacent tissues (P<0.05). Following the silencing of TEM8 by shRNA interference, cell proliferation was inhibited and the apoptosis rate increased. The cell cycle was arrested at G1 phase, while the migration and invasion ability of cancer cells was decreased. Silencing TEM8 may inhibit proliferation of XWLC‑05 lung cancer cells, promote cell apoptosis, arrest the cell cycle at G1 phase and decrease the migration and invasive ability. Thus, TEM8 may be a potential target in therapy for lung cancer.

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