TRPV2 channel negatively controls glioma cell proliferation and resistance to Fas-induced apoptosis in ERK-dependent manner

Nasopharyngeal carcinoma (NPC) is a common malignant head and neck tumor. Drug resistance and distant metastasis are the predominant cause of treatment failure in NPC patients. Hispidulin is a flavonoid extracted from the bioassay-guided separation of the EtOH extract of Salvia plebeia with strong anti-proliferative activity in nasopharyngeal carcinoma cells (CNE-2Z). In this study, the effects of hispidulin on proliferation, invasion, migration, and apoptosis were investigated in CNE-2Z cells. The [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] (MTT) assay and the colony formation assay revealed that hispidulin could inhibit CNE-2Z cell proliferation. Hispidulin (25, 50, 100 μM) also induced apoptosis in a dose-dependent manner in CNE-2Z cells. The expression of Akt was reduced, and the expression of the ratio of Bax/Bcl-2 was increased. In addition, scratch wound and transwell assays proved that hispidulin (6.25, 12.5, 25 μM) could inhibited the migration and invasion in CNE-2Z cells. The expressions of HIF-1α, MMP-9, and MMP-2 were decreased, while the MMPs inhibitor TIMP1 was enhanced by hispidulin. Moreover, hispidulin exhibited potent suppression tumor growth and low toxicity in CNE-2Z cancer-bearing mice at a dosage of 20 mg/kg/day. Thus, hispidulin appears to be a potentially effective agent for NPC treatment.

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microRNA-1296 Inhibits Glioma Cell Growth by Targeting ABL2

Technology in Cancer Research & Treatment ◽

10.1177/1533033821990009 ◽

2021 ◽

Vol 20 ◽

pp. 153303382199000

Author(s):

Gaolian Zhang ◽

Meng Xia ◽

Jianhui Guo ◽

Yi Huang ◽

Jianrong Huang ◽

...

Keyword(s):

Glioma Cell ◽

Karnofsky Performance Scale ◽

The Novel ◽

Inhibitory Effects ◽

Aberrant Expression ◽

Who Grade ◽

Glioma Cell Proliferation ◽

Mrna And Protein Expression ◽

Induced Apoptosis ◽

Tumor Suppressive Function

Aberrant expression of microRNAs (miRNAs) has been reported to play a role in tumorigenesis. Dysfunction of miR-1296 was found in a variety of cancers, however, the function of miR-1296 in the progression of glioma remains largely understood. Here, our results showed that miR-1296 was significantly down-regulated in glioma tissues and cell lines. Decreased expression of miR-1296 was associated with the tumor size, WHO grade and karnofsky performance scale (KPS) of glioma patients. Low expression of miR-1296 was significantly correlated with the shorter 5-year overall survival of glioma patients. Overexpression of miR-1296 inhibited the proliferation, colony formation, migration and induced apoptosis of glioma cells. MiR-1296 was found to bind the 3’-untranslated region (UTR) of ABL proto-oncogene 2 (ABL2) and subsequently repressed both the mRNA and protein expression of ABL2. ABL2 was overexpressed in glioma tissues and inversely correlated with that of miR-1296. Ectopic expressed ABL2 could reverse the inhibitory effects of miR-1296 on glioma cell proliferation. Our results illustrated the novel tumor-suppressive function of miR-1296 in glioma via repressing ABL2, suggesting a potential application of miR-1296 in the treatment of glioma.

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Correction to: MiR-126 Regulates the ERK Pathway via Targeting KRAS to Inhibit the Glioma Cell Proliferation and Invasion

Molecular Neurobiology ◽

10.1007/s12035-021-02302-3 ◽

2021 ◽

Author(s):

Yang Li ◽

Yunqian Li ◽

Pengfei Ge ◽

Chengyuan Ma

Keyword(s):

Cell Proliferation ◽

Glioma Cell ◽

Erk Pathway ◽

Glioma Cell Proliferation ◽

Proliferation And Invasion

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miR-25 promotes glioma cell proliferation by targeting CDKN1C

Biomedicine & Pharmacotherapy ◽

10.1016/j.biopha.2015.02.005 ◽

2015 ◽

Vol 71 ◽

pp. 7-14 ◽

Cited By ~ 24

Author(s):

Jihong Zhang ◽

Xuhai Gong ◽

Kaiyu Tian ◽

Dongkai Chen ◽

Jiahang Sun ◽

...

Keyword(s):

Cell Proliferation ◽

Glioma Cell ◽

Glioma Cell Proliferation

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NOTCH3 Is a Prognostic Factor That Promotes Glioma Cell Proliferation, Migration and Invasion via Activation of CCND1 and EGFR

PLoS ONE ◽

10.1371/journal.pone.0077299 ◽

2013 ◽

Vol 8 (10) ◽

pp. e77299 ◽

Cited By ~ 26

Author(s):

Mohammad A. Y. Alqudah ◽

Supreet Agarwal ◽

Maha S. Al-Keilani ◽

Zita A. Sibenaller ◽

Timothy C. Ryken ◽

...

Keyword(s):

Cell Proliferation ◽

Prognostic Factor ◽

Glioma Cell ◽

Migration And Invasion ◽

Glioma Cell Proliferation

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Blockage of Potassium Channel Inhibits Proliferation of Glioma Cells Via Increasing Reactive Oxygen Species

Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics ◽

10.3727/096504014x14098532393518 ◽

2014 ◽

Vol 22 (1) ◽

pp. 57-65 ◽

Cited By ~ 1

Author(s):

Li Hu ◽

Li-Li Li ◽

Zhi-Guo Lin ◽

Zhi-Chao Jiang ◽

Hong-Xing Li ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Cell Cycle ◽

Glioma Cell ◽

Glioma Cells ◽

Reactive Oxygen ◽

Dependent Manner ◽

Oxygen Species ◽

Brain Glioma ◽

Protein Levels ◽

Glioma Cell Proliferation

The potassium (K+) channel plays an important role in the cell cycle and proliferation of tumor cells, while its role in brain glioma cells and the signaling pathways remains unclear. We used tetraethylammonium (TEA), a nonselective antagonist of big conductance K+ channels, to block K+ channels in glioma cells, and antioxidant N-acetyl-l-cysteine (NAC) to inhibit production of intracellular reactive oxygen species (ROS). TEA showed an antiproliferation effect on C6 and U87 glioma cells in a time-dependent manner, which was accompanied by an increased intracellular ROS level. Antioxidant NAC pretreatment reversed TEA-mediated antiproliferation and restored ROS level. TEA treatment also caused significant increases in mRNA and protein levels of tumor-suppressor proteins p53 and p21, and the upregulation was attenuated by pretreatment of NAC. Our results suggest that K+ channel activity significantly contributes to brain glioma cell proliferation via increasing ROS, and it might be an upstream factor triggering the activation of the p53/p21Cip1-dependent signaling pathway, consequently leading to glioma cell cycle arrest.

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