CHD1L Regulates Cell Cycle, Apoptosis, and Migration in Glioma

Sun, Jie; Zhang, Li; Zhao, Hongyu; Qiu, Xiaojun; Chen, Wenjuan; Wang, Donglin; Ban, Na; Fan, Shaochen; Shen, Chaoyan; Xia, Xiaojie; Ji, Bin; Wang, Yuchan

doi:10.1007/s10571-015-0237-z

Cited by 19 publications

(13 citation statements)

References 33 publications

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“…Immunohistochemistry analysis was performed to examine the subcellular localization and expression pattern of SHMT2 protein in human glioma and non-neoplastic brain tissues according to the previous studies. 13 , 14 Following antigen retrieval, the sections were added with 0.3% hydrogen peroxide for 30 min to suppress endogenous peroxidase activities and blocked with 2% goat serum for 30 min. After that, the sections were blocked with 2% goat serum for 30 min and incubated overnight at 4°C with polyclonal rabbit anti-human SHMT2 antibody (1:150, ab180786; Abcam, Cambridge, MA, USA).…”

Section: Methodsmentioning

confidence: 99%

“…Two independent pathologists, who were both blinded to the patient background, were invited to evaluate SHMT2 immunostaining using immunoreactive score (IRS), which was calculated by multiplying the staining intensity and the positive cells’ percentage scores according to the previous studies. 13 , 14 Staining intensity was scored as follows: “0”, negative; “1”, weakly positive; “2”, moderately positive and “3”, strongly positive. The percentage of SHMT2-positive cells was scored as 0 (0%), 1 (1%–25%), 2 (26%–50%) and 3 (>50%).…”

Section: Methodsmentioning

confidence: 99%

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Overexpression of mitochondrial serine hydroxyl-methyltransferase 2 is associated with poor prognosis and promotes cell proliferation and invasion in gliomas

Wu¹,

Wanggou²,

Li³

et al. 2017

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Mitochondrial serine hydroxyl-methyltransferase 2 (SHMT2), participating in the synthesis of mitochondrial thymidine monophosphate, has been reported to drive glioma cell survival in ischemia. However, its clinical relevance in gliomas remains unclear. In the current study, immunohistochemistry was performed to examine subcellular localization and expression levels of SHMT2 protein in glioma and non-neoplastic brain tissue specimens. Then, the associations of SHMT2 expression with various clinicopathological features and patients’ prognosis were statistically evaluated. The roles of SHMT2 in the proliferation and invasion of glioma cells after siRNA-SHMT2 vector transfection were also detected by cell counting kit-8 and transwell assays, respectively. Results showed that SHMT2 immunostaining was predominantly localized in the cellular cytoplasm of tumor cells in glioma tissues but weakly in non-neoplastic brain tissues. Statistically, SHMT2 protein expression was significantly higher in glioma tissues than in non-neoplastic brain tissues (P<0.001). In addition, SHMT2 overexpression more frequently occurred in glioma patients with an advanced grade of malignancy (P<0.001) and poor prognosis (P=0.001). Notably, multivariate analysis based on a Cox regression model identified SHMT2 expression as an independent prognostic factor for glioma patients (P=0.01). Functionally, SHMT2 knockdown efficiently suppressed the proliferation (P=0.02) and invasion (P<0.001) of glioma cells in vitro. In conclusion, our findings suggest that SHMT2 may function as an oncogene in glioma development and progression. Clinically, SHMT2 may serve as a prognostic factor and as a potential therapeutic target for human gliomas.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Overexpression of mitochondrial serine hydroxyl-methyltransferase 2 is associated with poor prognosis and promotes cell proliferation and invasion in gliomas

Wu¹,

Wanggou²,

Li³

et al. 2017

OTT

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“…To assess the immunostaining results, two independent pathologists, who were both blinded to the patients’ background, were invited to score paxillin protein immunostaining based on staining intensity and positive cells’ percentage as described in previous studies 12,13. In brief, staining intensity was scored as follows: “0” negative, “1” weakly positive, “2” moderately positive, and “3” strongly positive.…”

Section: Methodsmentioning

confidence: 99%

Paxillin functions as an oncogene in human gliomas by promoting cell migration and invasion

Chen

Xia

et al. 2016

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BackgroundPaxillin is implicated in tumorigenesis, progression and aggressive phenotypes of various malignancies, highlighting its functions in cellular adhesion, migration and survival. However, the roles of paxillin in human gliomas remain unclear. The aim of this study was to evaluate the clinical implication of paxillin expression in patients with gliomas and its biological function in glioma cells.Patients and methodsExpression levels of paxillin gene and protein, respectively, were detected by quantitative real-time reverse transcription polymerase chain reaction, Western blot and immunohistochemistry analyses in 120 pairs of glioma and matched nontumorous brain tissues. The associations between paxillin expression and various histopathological features of glioma patients were also statistically evaluated. Then, the functions of paxillin in cell migration and invasion of glioma cell lines were determined by transwell assays in vitro.ResultsThe expression levels of both paxillin gene and protein in glioma tissues were markedly higher than those in matched nontumorous brain tissues. Notably, paxillin overexpression was significantly associated with the grade of malignancy (P<0.05). Moreover, the enforced expression of paxillin promoted the migration and invasion of glioma cells, while the loss of paxillin expression efficiently suppressed cell migration and invasion of glioma cell lines.ConclusionOur data suggest that paxillin may function as an oncogene and its overexpression may be closely correlated with tumor progression of human gliomas by modulating tumor cell motility, implying the potential of paxillin as a new therapeutic target for glioma intervention.

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“…In cancer cells, cell cycle alteration is a critical event which is closely related to the capability of proliferation, development, progression, resistance to treatment, and relapse. 32 Aberrant functioning of cell cycle regulators generally alters the properties of growth, differentiation, and apoptosis in cancer cells. 33 The increased ratio of G1 phase population hints that the knockdown of PCGF1 could prevent U87 cells progressing from G0/G1 to S phase, and consequently, decrease the activity of cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

<p>Repression of PCGF1 Decreases the Proliferation of Glioblastoma Cells in Association with Inactivation of c-Myc Signaling Pathway</p>

Yan¹,

Cui²,

Dong³

et al. 2020

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Glioblastoma (GBM) is the most common primary brain tumor with a poor therapeutic outcome. Polycomb group factor 1 (PCGF1), a member of the PcG (Polycomb group) family, is highly expressed in the developing nervous system of mice. However, the function and the mechanism of PCGF1 in GBM proliferation still remain unclear. Methods: Knockdown of PCGF1 was performed in U87 GBM cell by shRNA strategy via lentivirus vector. MTT assay, colony formation assays, and flow cytometry were used to measure the properties of cell proliferation and cell cycle distribution, respectively. GeneChip analysis was performed to identify the downstream effector molecules. Rescue assay was constructed to verify the screening results. Results: We first found that knockdown of PCGF1 led to the inhibition of U87 cells proliferation and decreased colony formation ability. The data from GeneChip expression profiling and Ingenuity Pathway Analysis (IPA) indicated that many of the altered gene cells are associated with the cell proliferation control pathways. We have further confirmed the suppression of AKT/ GSK3β/c-Myc/cyclinD1 expressions by Western blotting analysis. The over-expression of c-Myc could partly restore the attenuated proliferation ability caused by knockdown of PCGF1. Conclusion: All the above evidences suggested that PCGF1 might be closely associated with tumorigenesis and progression of glioblastoma (GBM), in which process the oncoprotein c-Myc may participate. PCGF1 could thus be a potential therapeutic target for the treatment of glioblastoma (GBM).

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CHD1L Regulates Cell Cycle, Apoptosis, and Migration in Glioma

Cited by 19 publications

References 33 publications

Overexpression of mitochondrial serine hydroxyl-methyltransferase 2 is associated with poor prognosis and promotes cell proliferation and invasion in gliomas

Overexpression of mitochondrial serine hydroxyl-methyltransferase 2 is associated with poor prognosis and promotes cell proliferation and invasion in gliomas

Paxillin functions as an oncogene in human gliomas by promoting cell migration and invasion

<p>Repression of PCGF1 Decreases the Proliferation of Glioblastoma Cells in Association with Inactivation of c-Myc Signaling Pathway</p>

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