Should oncologists measure the mRNA and protein expression levels of ERCC1 and RRM1 in non-small-cell lung cancer?

2007 ◽  
Vol 4 (10) ◽  
pp. 564-565
Author(s):  
Rebecca S Heist ◽  
Geoffrey Liu ◽  
Wei Zhou
Keyword(s):  
Lung Cancer ◽  
Protein Expression ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Expression Levels ◽  
Mrna And Protein Expression

scholarly journals CACNA1B (Cav2.2) Overexpression and Its Association with Clinicopathologic Characteristics and Unfavorable Prognosis in Non-Small Cell Lung Cancer

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Xiaoyu Zhou ◽  
Wei Wang ◽  
Shu Zhang ◽  
Xudong Wang ◽  
Zhiyuan Tang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Expression ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Underlying Mechanism ◽  
Small Cell ◽  
Small Cell Lung ◽  
Clinicopathologic Characteristics ◽  
Incidence And Mortality ◽  
Mrna And Protein Expression

CACNA1B (Cav2.2) encodes an N-type voltage-gated calcium channel (VGCC) ubiquitously expressed in brain and peripheral nervous system that is important for regulating neuropathic pain. Because intracellular calcium concentration is a key player in cell proliferation and apoptosis, VGCCs are implicated in tumorigenesis. Recent studies have identified CACNA1B (Cav2.2) being overexpressed in prostate and breast cancer tissues when compared to adjacent normal tissues; however, its role in non-small cell lung cancer (NSCLC) has not been investigated. In this study, we determined the mRNA and protein expression of CACNA1B (Cav2.2) in NSCLC tumorous and adjacent nontumorous tissues by quantitative reverse transcription PCR (qRT-PCR) and tissue microarray immunohistochemistry analysis (TMA-IHC), respectively. CACNA1B (Cav2.2) protein expressions in tumorous tissues were correlated with NSCLC patients’ clinical characteristics and overall survival. CACNA1B (Cav2.2) mRNA and protein expression levels were higher in NSCLC tumorous tissues than in nontumorous tissues. High CACNA1B (Cav2.2) protein expression was associated with higher TNM stages, and CACNA1B (Cav2.2) protein expression is an independent prognostic marker in NSCLC. Based on our results, we conclude that CACNA1B (Cav2.2) plays a role in NSCLC development and progression. Elucidating the underlying mechanism may help design novel treatment by specifically targeting the calcium regulation pathway for NSCLC, a devastating disease with increasing incidence and mortality in China.

lncRNAs as Potential Targets in Small Cell Lung Cancer: MYC -dependent Regulation

2020 ◽  
Vol 20 (17) ◽  
pp. 2074-2081
Author(s):  
Onur Tokgun ◽  
Pervin E. Tokgun ◽  
Kubilay Inci ◽  
Hakan Akca
Keyword(s):  
Lung Cancer ◽  
Stem Cell ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Therapeutic Strategy ◽  
Small Cell ◽  
Small Cell Lung ◽  
Expression Levels ◽  
Qrt Pcr ◽  
Shrna Vector

Background: Small Cell Lung Cancer (SCLC) is a highly aggressive malignancy. MYC family oncogenes are amplified and overexpressed in 20% of SCLCs, showing that MYC oncogenes and MYC regulated genes are strong candidates as therapeutic targets for SCLC. c-MYC plays a fundamental role in cancer stem cell properties and malignant transformation. Several targets have been identified by the activation/repression of MYC. Deregulated expression levels of lncRNAs have also been observed in many cancers. Objective: The aim of the present study is to investigate the lncRNA profiles which depend on MYC expression levels in SCLC. Methods: Firstly, we constructed lentiviral vectors for MYC overexpression/inhibition. MYC expression is suppressed by lentiviral shRNA vector in MYC amplified H82 and N417 cells, and overexpressed by lentiviral inducible overexpression vector in MYC non-amplified H345 cells. LncRNA cDNA is transcribed from total RNA samples, and 91 lncRNAs are evaluated by qRT-PCR. Results: We observed that N417, H82 and H345 cells require MYC for their growth. Besides, MYC is not only found to regulate the expressions of genes related to invasion, stem cell properties, apoptosis and cell cycle (p21, Bcl2, cyclinD1, Sox2, Aldh1a1, and N-Cadherin), but also found to regulate lncRNAs. With this respect, expressions of AK23948, ANRIL, E2F4AS, GAS5, MEG3, H19, L1PA16, SFMBT2, ZEB2NAT, HOTAIR, Sox2OT, PVT1, and BC200 were observed to be in parallel with MYC expression, whereas expressions of Malat1, PTENP1, Neat1, UCA1, SNHG3, and SNHG6 were inversely correlated. Conclusion: Targeting MYC-regulated genes as a therapeutic strategy can be important for SCLC therapy. This study indicated the importance of identifying MYC-regulated lncRNAs and that these can be utilized to develop a therapeutic strategy for SCLC.

Protein expression of close homologue of L1 (CHL1) is a marker for overall survival in non-small cell lung cancer (NSCLC)

2019 ◽  
Vol 145 (9) ◽  
pp. 2285-2292 ◽  
Author(s):  
Jenny Hötzel ◽  
Nathaniel Melling ◽  
Julia Müller ◽  
Adam Polonski ◽  
Gerrit Wolters-Eisfeld ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Overall Survival ◽  
Protein Expression ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Close Homologue

P-652 Protein expression profiles in non-small cell lung cancer. A tissue microarray-based study of 142 cases

Lung Cancer ◽  
2005 ◽  
Vol 49 ◽  
pp. S290 ◽  
Author(s):  
E. Conde ◽  
R. García Luján ◽  
A. López Encuentra ◽  
L. Sánchez ◽  
M. Sánchez-Céspedes ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Expression ◽  
Small Cell Lung Cancer ◽  
Tissue Microarray ◽  
Cell Lung Cancer ◽  
Expression Profiles ◽  
Small Cell ◽  
Small Cell Lung ◽  
Protein Expression Profiles

scholarly journals KIR 2D (L1, L3, L4, S4) and KIR 3DL1 protein expression in non-small cell lung cancer

Oncotarget ◽  
2016 ◽  
Vol 7 (50) ◽  
pp. 82104-82111 ◽  
Author(s):  
Yayi He ◽  
Paul A. Bunn ◽  
Caicun Zhou ◽  
Dan Chan
Keyword(s):  
Lung Cancer ◽  
Protein Expression ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung

Cigarette Smoke-Induced Reduction of 14-3-3σ Expression Promotes The Progression of Non-Small Cell Lung Cancer

2021 ◽  
Author(s):  
Longxia Dai ◽  
Quanwen Deng ◽  
Aibin Liu ◽  
Shuya He ◽  
Qiong Chen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Expression ◽  
Small Cell Lung Cancer ◽  
Cigarette Smoke ◽  
Cell Lung Cancer ◽  
A549 Cells ◽  
Small Cell ◽  
Small Cell Lung ◽  
Smoking Group ◽  
The Relationship

Abstract Background Lung cancer is a common malignant tumour and the leading cause of cancer death. Smoking is closely related to lung cancer, which can not only induce the occurrence of lung cancer but also affect its progress and prognosis. Objectives To investigated the relationship between smoking and 14-3-3σ protein expression in non-small-cell lung cancer (NSCLC), investigated the relationship between 14-3-3σ expression and cell migration in A549 cells induced by cigarette smoke extract (CSE) and explored whether DNA methylation plays a role in the decreased expression of 14-3-3σ induced by CSE. Methods 14-3-3σ protein expression was examined by immunohistochemistry in 152 NSCLC tissue samples. In vitro experiments were divided into three groups: The current smoking group (CS), the ex-smoking group (ES) and the normal control group (NC). Cell transfection was used for 14-3-3σ protein overexpression. The mRNA and protein expression levels of 14-3-3σ were detected by RT-PCR and Western blotting, respectively. Cell migration was detected by Transwell and wound-healing assays, and the methylation of 14-3-3σ was detected by methylation-specific PCR. Results 14-3-3σ protein expression was decreased in NSCLC patients with a history of smoking. The expression of 14-3-3σ was decreased in A549 cells treated with CSE. The migration capacity of A549 cells treated with CSE was enhanced. DNA methylation in the cigarette smoke-treated A549 cells was higher than that in the untreated cells. Conclusion Cigarette smoke induced reduction of 14-3-3σ expression can promote the progression of non-small cell lung cancer.

scholarly journals Inhibition of HERG1 K+ channel protein expression decreases cell proliferation of human small cell lung cancer cells

2011 ◽  
Vol 463 (2) ◽  
pp. 365-376 ◽  
Author(s):  
Günter Glassmeier ◽  
Kathrin Hempel ◽  
Iris Wulfsen ◽  
Christiane K. Bauer ◽  
Udo Schumacher ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
K Channel ◽  
Small Cell Lung

scholarly journals Circ_MDM2_000139, Circ_ATF2_001418, Circ_CDC25C_002079, and Circ_BIRC6_001271 Are Involved in the Functions of XAV939 in Non-Small Cell Lung Cancer

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Haixiang Yu ◽  
Lei Xu ◽  
Zhengjia Liu ◽  
Bo Guo ◽  
Zhifeng Han ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Regulatory Network ◽  
Family Members ◽  
Enrichment Analysis ◽  
Small Cell ◽  
Small Cell Lung ◽  
Expression Levels ◽  
Relative Expression

Background. The small molecule inhibitor XAV939 could inhibit the proliferation and promote the apoptosis of non-small cell lung cancer (NSCLC) cells. This study was conducted to identify the key circular RNAs (circRNAs) and microRNAs (miRNAs) in XAV939-treated NSCLC cells. Methods. After grouping, the NCL-H1299 cells in the treatment group were treated by 10 μM XAV939 for 12 h. RNA-sequencing was performed, and then the differentially expressed circRNAs (DE-circRNAs) were analyzed by the edgeR package. Using the clusterprofiler package, enrichment analysis for the hosting genes of the DE-circRNAs was performed. Using Cytoscape software, the miRNA-circRNA regulatory network was built for the disease-associated miRNAs and the DE-circRNAs. The DE-circRNAs that could translate into proteins were predicted using circBank database and IRESfinder tool. Finally, the transcription factor (TF)-circRNA regulatory network was built by Cytoscape software. In addition, A549 and HCC-827 cell treatment with XAV939 were used to verify the relative expression levels of key DE-circRNAs. Results. There were 106 DE-circRNAs (including 61 upregulated circRNAs and 45 downregulated circRNAs) between treatment and control groups. Enrichment analysis for the hosting genes of the DE-circRNAs showed that ATF2 was enriched in the TNF signaling pathway. Disease association analysis indicated that 8 circRNAs (including circ_MDM2_000139, circ_ATF2_001418, circ_CDC25C_002079, and circ_BIRC6_001271) were correlated with NSCLC. In the miRNA-circRNA regulatory network, let-7 family members⟶circ_MDM2_000139, miR-16-5p/miR-134-5p⟶circ_ATF2_001418, miR-133b⟶circ_BIRC6_001271, and miR-221-3p/miR-222-3p⟶circ_CDC25C_002079 regulatory pairs were involved. A total of 47 DE-circRNAs could translate into proteins. Additionally, circ_MDM2_000139 was targeted by the TF POLR2A. The verification test showed that the relative expression levels of circ_MDM2_000139, circ_CDC25C_002079, circ_ATF2_001418, and circ_DICER1_000834 in A549 and HCC-827 cell treatment with XAV939 were downregulated comparing with the control. Conclusions. Let-7 family members and POLR2A targeting circ_MDM2_000139, miR-16-5p/miR-134-5p targeting circ_ATF2_001418, miR-133b targeting circ_BIRC6_001271, and miR-221-3p/miR-222-3p targeting circ_CDC25C_002079 might be related to the mechanism in the treatment of NSCLC by XAV939.

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