Knockdown of OCT4 may sensitize NSCLC cells to cisplatin

Liu, X.; Ma, Mingquan; Duan, Xiaofeng; Zhang, H.; Yang, Manyi

doi:10.1007/s12094-016-1569-y

Cited by 19 publications

(12 citation statements)

References 15 publications

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“…Maybe Cisplatin (8 μg/ml) still could affect other pro-apoptosis genes that could induce cell apoptosis. Similarly, Liu et al’s [44] research also supported ours. And a more in-depth research will be launched in the future study to explain this result clearly.…”

Section: Discussionsupporting

confidence: 88%

Down-regulation of CCNE1 expression suppresses cell proliferation and sensitizes gastric carcinoma cells to Cisplatin

Zhang

Zhu

et al. 2019

Bioscience Reports

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A novel oncogene CCNE1 (cyclin E) is considered to be associated with the development of various tumor types, its role in gastric carcinoma (GC) is little studied and the effect of CCNE1 on chemotherapy also remains unclear. We recruited 55 cases of GC tissues and corresponding normal tissues. Immunohistochemistry (IHC), quantitative real-time PCR (qRT-PCR) and Western blot analysis were performed to detect the expression of CCNE1. We also examined the expression of CCNE1 in gastric mucosal GES-1 cells and five GC cell lines. Silencing CCNE1 was used to assess its effect on proliferation and cell cycle in MGC-803 and NCI-N87 cells, as performed by Cell counting kit-8 (CCK-8) and flow cytometry assay. Meanwhile, cell cycle related genes were also detected through qRT-PCR and Western blot. The results showed CCNE1 up-regulation mainly expressed in GC tissues and GC cell lines, also was associated with tumor node metastasis (TNM) stage and lymphatic invasion. Three-year survival curve analysis showed CCNE1 with high expression had a poor prognosis. Silencing CCNE1 significantly reduced cell viability in 48 h, cultured and arrested cell cycle in G1 phase, moreover, Cyclin A, D1 and C-myc all revealed down-regulation in both MGC-803 and NCI-N87 cells. CCNE1 expression was significantly increased at low and moderate concentrations of Cisplatin. Down-regulation of CCNE1 expression would remarkably promote cell apoptosis induced by Cisplatin, and regulate the rate of Bax/Bcl-2. Down-regulation of CCNE1 expression could inhibit cell proliferation and enhance GC cells sensibility to Cisplatin, possibly involving the regulation of Bcl-2 family.

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Section: Discussionsupporting

confidence: 88%

Down-regulation of CCNE1 expression suppresses cell proliferation and sensitizes gastric carcinoma cells to Cisplatin

Zhang

Zhu

et al. 2019

Bioscience Reports

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“…Moreover, Oct4 downregulation has been strongly associated with cancer invasion suppression [47–49] and chemosensitization [50] in different neoplasms, which indicates that Oct4 could be useful as a therapeutic target.…”

Section: Discussionmentioning

confidence: 99%

High Oct4 expression: implications in the pathogenesis of neuroblastic tumours

Monferrer¹,

et al. 2019

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BackgroundNeuroblastic tumours (NBTs) are paediatric solid tumours derived from embryonic neural crest cells which harbour their own cancer stem cells (CSC). There is evidence indicating that CSC may be responsible for tumour progression, chemotherapy resistance and recurrence in NBTs. Oct4 is a transcription factor which plays a key role in mammal embryonic development and stem cell fate regulation. The aim of the study is to elucidate the clinical significance of Oct4 in NBTs.MethodsWe studied Oct4 expression in 563 primary NBTs using digital image quantification. Chi-square test was applied to analyse the correlation between histopathology and the Oct4+ cell percentage. Survival analysis was carried out with Kaplan-Meier curves and log-rank test. Additionally, a multivariate Cox regression analysis with the stepwise backwards (Wald) method was undertaken to calculate the impact of Oct4 expression level on survival.ResultsWe found that tumours with a high proportion of cells expressing Oct4 correlated statistically with undifferentiated and poorly differentiated neuroblastoma / nodular ganglioneuroblastoma, and that Oct4 expression was not present in ganglioneuroma (p < 0.05). Statistical analysis also indicated a relationship between high Oct4 expression levels, high-risk patients according to the International Neuroblastoma Risk Group pre-treatment classification parameters, larger blood vessels and low survival rates.ConclusionsThese results suggest that the Oct4 gene may regulate NBT pathogenic differentiation pathways, and should thus be considered as a target for knockdown when developing novel therapies for high-risk NBT patients.

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“…Elevated OCT4 expression has been reported in many tumor types including NSCLC, and the expression levels of OCT4 mRNA and protein were significantly higher in tumor tissues compared with adjacent normal tissues [7]. Researchers revealed that OCT4 is linked to chemoresistance to cisplatin in NSCLC cells, suggesting that OCT4 inhibition may be a potential strategy for chemosensitization of NSCLC cells [8]. Clinical studies further validated the importance of the OCT4/NEAT1/MALAT1 signaling axis in lung cancer progression [9].…”

Section: Introductionmentioning

confidence: 97%

Association of Single-Nucleotide Polymorphism REX1 rs6815391, OCT4 rs13409 or rs3130932, and CTBP2 rs3740535 with Primary Lung Cancer Susceptibility: A Case-Control Study in a Chinese Population

Shen

Wang

et al. 2019

Disease Markers

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The purpose of the current study is to explore the contribution of single-nucleotide polymorphisms (SNPs) of REX1 rs6815391, OCT4 rs13409 or rs3130932, and CTBP2 rs3740535 to the risk of lung cancer. A questionnaire survey was used to obtain basic information of the included subjects. A case control study was performed in 1121 patients and 1121 controls. All subjects were subjected to blood sampling for genomic DNA extraction and genotyping of the cancer stem cell-associated gene SNPs, including REX1 rs6815391, OCT4 rs13409 or rs3130932, and CTBP2 rs3740535 by real-time PCR. The association with the risk of primary lung cancer and interaction with environmental factors were assessed using unconditional logistic regression for the odds ratios and corresponding 95% confidence intervals. The genotype frequency distribution of OCT4 rs13409 loci was statistically significant, but there was no significant difference in the rest of the loci between lung cancer patients and healthy controls. The OCT4 gene was also related with lung cancer susceptibility in the genetic model after adjusting for lung cancer-related factors. Despite the presence of the dominant or recessive model, the four loci polymorphisms were associated with pollution near the place of residence, house type, worse ventilation situation, smoking, passive smoking, cooking oil fumes (COF), and family history of cancer, which increased the risk of lung cancer. Nonmarried status, 18.5≤BMI, COF, smoking, passive smoking, family history of cancer, and history of lung disease were independent risk factors of lung cancer susceptibility. Additionally, college degree or above, no pollution near the place of residence, protective genotype 1 or 2, and well ventilation can reduce the occurrence of lung cancer. There is an interaction between the four loci and environmental factors, and OCT4 rs13409 is a risk factor of primary lung cancer.

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Knockdown of OCT4 may sensitize NSCLC cells to cisplatin

Abstract: Our findings indicate that targeting OCT4 could improve cisplatin effect in NSCLC, confirming their role in modulating cisplatin sensitivity.

Cited by 19 publications

References 15 publications

Down-regulation of CCNE1 expression suppresses cell proliferation and sensitizes gastric carcinoma cells to Cisplatin

Down-regulation of CCNE1 expression suppresses cell proliferation and sensitizes gastric carcinoma cells to Cisplatin

High Oct4 expression: implications in the pathogenesis of neuroblastic tumours

Association of Single-Nucleotide Polymorphism REX1 rs6815391, OCT4 rs13409 or rs3130932, and CTBP2 rs3740535 with Primary Lung Cancer Susceptibility: A Case-Control Study in a Chinese Population

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