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07 January 2016 : Clinical Research  

Expression of Tim4 in Glioma and its Regulatory Role in LN-18 Glioma Cells

Weiguo LiDE, Xingang LiABC, Shujun XuFG, Xiangyu MaEG, Qiujie ZhangAG

DOI: 10.12659/MSM.894963

Med Sci Monit 2016; 22:77-82


BACKGROUND: Tim4 is a transmembrane protein known as T cell immunoglobulin and mucin domain containing protein-4. We speculated that Tim4 might be associated with glioma. This study aimed to investigate the expression level of Tim4 in gliomas and the regulatory role of Tim4 on the growth and apoptosis of LN-18 glioma cells.

MATERIAL AND METHODS: Tumor tissues and adjacent normal tissues were collected from patients with glioma. The expression level of Tim4 mRNA and protein was determined by RT-PCR and Western blot analyses, respectively to evaluate their association with glioma. Tim4 was overexpressed or silenced by siRNA interference in cultured human glioma cells LN-18. The growth and apoptosis of LN-18 cells was detected by MTT assay and flow cytometry. The colony-forming ability of LN-18 cells was assessed by the colony formation assay. The collection of human tissues was approved by the Research Ethics Committee at the Harbin Medical University Cancer Hospital and performed in strict accordance with international standards. All patients were required to sign the informed consent.

RESULTS: The expression level of Tim4 mRNA and protein in tumor tissues was significantly higher compared with adjacent normal tissues. Antisense miRNA targeting Tim4 inhibited the growth of LN-18 cells, induced their apoptosis, and reduced their clonogenic capacity. In contrast, overexpression of Tim4 promoted the growth of LN-18 cells, inhibited their apoptosis, and enhanced their clonogenic potential.

CONCLUSIONS: The expression level of Tim-4 is closely associated with glioma. Decreased expression of Tim4 inhibited the growth and colony-forming ability of LN-18 cells and induced their apoptosis, whereas increased expression of Tim4 stimulated the growth and clonogenic potential of LN-18 cells and suppressed their apoptosis.

Keywords: Brain Neoplasms - metabolism, Gene Expression Profiling, Glioma - metabolism, Membrane Proteins - metabolism, RNA Interference, RNA, Messenger - metabolism, RNA, Small Interfering - metabolism

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Dinah V. Parums
Science Editor, Medical Science Monitor, International Scientific Information, Inc., Melville, NY, USA

DOI: 10.12659/MSM.943312

Med Sci Monit 2023; 29:e943312

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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750