Abstract
Proteolipid protein 2 (PLP2), a membrane protein of the endoplasmic reticulum, is related to tumor proliferation and metastasis in some human cancers, but not in gliomas. First, we performed western-blot analysis, real-time quantitative PCR and immunohistochemical stains to detect PLP2 expression in 4 glioma cell lines and human glioma tissues. In addition, we used small interfering RNA (SiPLP2) and short hairpin RNA (shPLP2) to knockdown PLP2 expression in GBM8401 and LN229 glioma cell lines. After then, the alteration of PLP2 suppressed glioma cells behavior were examined by cell proliferation, wound healing, cell invasion, and colonies formation assays. Finally, the possible mechanism of PLP2 was analyzed by detecting the expression of the proteins related to cell-cycle checkpoints, cell-proliferative signaling factors, and cell-matrix interaction. Compared with normal brain cell lysates and mRNA, all glioma cell lines displayed PLP2 protein and mRNA overexpression. Besides, higher PLP2 IHC staining significantly correlated with more advanced tumor grades and poorer prognosis in human gliomas. Both siPLP2 transfected gliomas showed a clear inhibition of glioma cell proliferation, migration, and invasion as well as down-regulating p-p38, p-ERK, MMP-2, and MMP-9 expression. In conclusion, we successfully demonstrated that PLP2 overexpression played an oncogenic role in glioma development and aggressive tumor behavior.
Highlights
Primary brain tumors (PBT) are not -identified neoplasms because of the limitations of diagnostic tools and the inconspicuous symptoms, except for tumor compression [1]
To detect Proteolipid protein 2 (PLP2) protein expression, western-blot analysis was performed in normal brain tissue and human glioma cell lines
Compared with normal brain cell lysates, our study revealed PLP2 overexpression in the GBM8401, LN229, U87MG, and U118MG human glioma cell lines (* p < 0.05; ** p < 0.01; *** p < 0.001, Figure 1A)
Summary
Primary brain tumors (PBT) are not -identified neoplasms because of the limitations of diagnostic tools and the inconspicuous symptoms, except for tumor compression [1]. The concomitance of newly developed alkylating drugs, such as temozolomide (TMZ), with external beam radiation therapy or stereotactic radiosurgery has been shown to effectively induce apoptosis in high-grade glioma cells and potentially result in prognostic improvement. This concomitance is especially apparent in elderly patients [7,8]. Many genetic mutations have been proven to be related to drug effectiveness and the disease-free survival of glioma patients Such mutations include those of O6 methyl-guanine methyltransferase (MGMT) [15,16], isocitrate dehydrogenase (IDH) [17,18], BRAF [19,20], and co-deletion of 1p and 19q [21,22,23]. PBTs are considered a multifactorial disease [5]
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