scholarly journals Systematic analysis of mRNA expression profiles in NSCLC cell lines to screen metastasis-related genes

2016 ◽  
Vol 14 (6) ◽  
pp. 5093-5103 ◽  
Author(s):  
Ying Liu ◽  
Lei Liu ◽  
Tao Yu ◽  
He-Chun Lin ◽  
Dandan Chu ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Cell Lines ◽  
Expression Profiles ◽  
Nsclc Cell ◽  
Systematic Analysis

scholarly journals Expression Profiles of microRNAs in Drug-Resistant Non-Small Cell Lung Cancer Cell Lines Using microRNA Sequencing

2018 ◽  
Vol 51 (6) ◽  
pp. 2509-2522 ◽  
Author(s):  
Shousen Hu ◽  
Yongliang Yuan ◽  
Zhizhen Song ◽  
Dan Yan ◽  
Xiangzhen Kong
Keyword(s):  
Lung Cancer ◽  
Drug Resistance ◽  
Small Cell Lung Cancer ◽  
Cell Lines ◽  
Cell Lung Cancer ◽  
Expression Profiles ◽  
Small Cell ◽  
Nsclc Cell ◽  
Drug Resistant ◽  
Small Cell Lung

Background/Aims: Drug resistance remains a main obstacle to the treatment of non- small cell lung cancer (NSCLC). The aim of this study was to identify the expression profiles of microRNAs (miRNAs) in drug-resistant NSCLC cell lines. Methods: The expression profiles of miRNAs in drug-resistant NSCLC cell lines were examined using miRNA sequencing, and the common dysregulated miRNAs in these cell lines were identified and analyzed by bioinformatics methods. Results: A total of 29 upregulated miRNAs and 36 downregulated miRNAs were found in the drug-resistant NSCLC cell lines, of which 26 upregulated and 36 downregulated miRNAs were found to be involved in the Ras signaling pathway. The expression levels, survival analysis, and receiver operating characteristic curve of the dysregulated miRNAs based on The Cancer Genome Atlas database for lung adenocarcinoma showed that hsa-mir-192, hsa-mir-1293, hsa-mir-194, hsa-mir-561, hsa-mir-205, hsa-mir-30a, and hsa-mir-30c were related to lung cancer, whereas only hsa-mir-1293 and hsa-mir-561 were not involved in drug resistance. Conclusion: The results of this study may provide novel biomarkers for drug resistance in NSCLC and potential therapies for overcoming drug resistance, and may also reveal the potential mechanisms underlying drug resistance in this disease.

scholarly journals Comprehensive RNA analysis of CSF reveals a role for CEACAM6 in lung cancer leptomeningeal metastases

2021 ◽  
Vol 5 (1) ◽  
Author(s):  
Yingmei Li ◽  
Dina Polyak ◽  
Layton Lamsam ◽  
Ian David Connolly ◽  
Eli Johnson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Single Cell ◽  
Cell Lines ◽  
Expression Profiles ◽  
Leptomeningeal Metastases ◽  
Detection Sensitivity ◽  
Nsclc Cell ◽  
Rna Seq ◽  
The Brain

AbstractNon-small cell lung cancer (NSCLC) metastatic to the brain leptomeninges is rapidly fatal, cannot be biopsied, and cancer cells in the cerebrospinal fluid (CSF) are few; therefore, available tissue samples to develop effective treatments are severely limited. This study aimed to converge single-cell RNA-seq and cell-free RNA (cfRNA) analyses to both diagnose NSCLC leptomeningeal metastases (LM), and to use gene expression profiles to understand progression mechanisms of NSCLC in the brain leptomeninges. NSCLC patients with suspected LM underwent withdrawal of CSF via lumbar puncture. Four cytology-positive CSF samples underwent single-cell capture (n = 197 cells) by microfluidic chip. Using robust principal component analyses, NSCLC LM cell gene expression was compared to immune cells. Massively parallel qPCR (9216 simultaneous reactions) on human CSF cfRNA samples compared the relative gene expression of patients with NSCLC LM (n = 14) to non-tumor controls (n = 7). The NSCLC-associated gene, CEACAM6, underwent in vitro validation in NSCLC cell lines for involvement in pathologic behaviors characteristic of LM. NSCLC LM gene expression revealed by single-cell RNA-seq was also reflected in CSF cfRNA of cytology-positive patients. Tumor-associated cfRNA (e.g., CEACAM6, MUC1) was present in NSCLC LM patients’ CSF, but not in controls (CEACAM6 detection sensitivity 88.24% and specificity 100%). Cell migration in NSCLC cell lines was directly proportional to CEACAM6 expression, suggesting a role in disease progression. NSCLC-associated cfRNA is detectable in the CSF of patients with LM, and corresponds to the gene expression profile of NSCLC LM cells. CEACAM6 contributes significantly to NSCLC migration, a hallmark of LM pathophysiology.

scholarly journals The Stable 2.0-Kilobase Intron of the Herpes Simplex Virus Type 1 Latency-Associated Transcript Does Not Function as an Antisense Repressor of ICP0 in Nonneuronal Cells

2003 ◽  
Vol 77 (6) ◽  
pp. 3516-3530 ◽  
Author(s):  
Edward A. Burton ◽  
Chang-Sook Hong ◽  
Joseph C. Glorioso
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Mrna Expression ◽  
Cell Lines ◽  
Expression Profiles ◽  
Early Gene ◽  
Wild Type Virus ◽  
Wild Type ◽  
Viral Mutant ◽  
Simplex Virus

ABSTRACT During latency, herpes simplex virus expresses a unique set of latency-associated transcripts (LATs). As the 2.0-kb LAT intron is complementary to, and overlaps, the 3′ end of the ICP0 transcript, it has been suggested that the stable LAT intron might function as an antisense repressor of ICP0 expression. We tested this hypothesis in cell culture by dissociating cis- and trans-acting effects of the 2.0-kb LAT, using a series of complementary strategies. Initially, we constructed 293T cell lines that stably express the nuclear 2.0-kb LAT intron to determine whether LAT accumulation in trans affects ICP0 expression. ICP0 mRNA and protein expression profiles were studied (i) following infections with a viral mutant containing wild-type LAT and ICP0 sequences but having deletions of other immediate-early (IE) genes, thus preventing the progression of viral early gene expression, (ii) at early time points after infection with wild-type virus, before viral LAT expression, and (iii) by plasmid transfections. Northern and Western blot analysis showed that trans expression of the 2.0-kb LAT intron does not affect ICP0 mRNA expression, stability, accumulation, splicing, or translation. In addition, suppression of viral replication by overexpression of the 2.0-kb LAT, which has been detected previously in neuronal cell lines, was not found in these nonneuronal cell lines. However, deletion of the latency-active promoter (LAP) region of the virus resulted in overexpression of IE genes, which occurred soon after infection, before viral LAT expression had commenced. This was not complemented by the expression of LAT in trans, suggesting that the LAP deletion affected transcriptional regulation of the IE genes in cis. We conclude that the function of the highly conserved LAT intron is unlikely to involve a direct-acting anti-ICP0 antisense mechanism but that the LAT region could affect ICP0 mRNA expression from the viral genome.

DEAH-Box Splicing Factor Gene, Prp16 Amplification in Acute Myeloid Leukemia.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4479-4479
Author(s):  
Yupo Ma ◽  
Tammy Barnett ◽  
Li Chai ◽  
Jianchang Yang ◽  
Zaida Alipio ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Mrna Expression ◽  
Cell Lines ◽  
Myeloid Leukemia ◽  
Expression Profiles ◽  
Mrna Splicing ◽  
Splicing Factor ◽  
Aberrant Expression ◽  
Factor Gene ◽  
Acute Myeloid

Abstract Aberrant mRNA splicing has been observed frequently in solid tumors and shown to play a functionally significant role in tumorgenesis. Here we demonstrate that the DEAH-Box splicing factor gene, Prp16, is amplified in fresh human acute myeloid leukemia (AML) and in established AML cell lines. Prp16, an RNA-dependent ATPase required for pre-mRNA splicing, maps to chromosome 16q22, a region frequently altered in AML. Amplification of the Prp16 gene was initially detected using digital karyotyping, a powerful technique for analyzing genome-wide alterations in DNA copy number and verified by quantitative real-time PCR. Analysis of mRNA expression profiles revealed that Prp16 transcripts were present at high levels in 22 of 39 cases of AML (56%) and in both AML cell lines examined. There was a strong correlation between gene amplification and mRNA expression levels. To our knowledge, this is the first demonstration linking aberrant expression of a splicing enzyme to leukemogenesis. The classification and clinical outcome of the AML cases is being correlated with the presence or absence of Prp16 amplification. The identification of leukemia-specific splicing event(s) may provide a novel target for therapeutic intervention.

Characteristics of NSCLCs harboring NRAS mutations.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 7532-7532
Author(s):  
Kadoaki Ohashi ◽  
Lecia V. Sequist ◽  
Martin Sos ◽  
Xi Chen ◽  
Charles M. Rudin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Cell Lines ◽  
Expression Profiles ◽  
Nsclc Cell ◽  
Disease Stage ◽  
Smoking History ◽  
Egfr Mutations ◽  
Targeted Agents ◽  
Mek Inhibitors

7532 Background: We sought to determine the frequency and clinical characteristics of patients with non-small cell lung cancers (NSCLCs) harboring NRAS mutations. We used preclinical models to identify targeted therapies likely to be of benefit against NRAS mutant lung cancer cells. Methods: We reviewed data in the Catalogue of Somatic Mutations in Cancer (COSMIC) and clinical history from patients with NSCLC whose tumors underwent systematic screening for driver mutations including NRAS. Patient characteristics examined included age, gender, race, smoking history, disease stage, treatment history, and overall survival (OS). 6 NSCLC cell lines with NRAS mutations were screened for sensitivity against multiple targeted agents. Gene expression was profiled using Affymetrix U133A arrays in 5 NRAS mutant NSCLC cell lines, 8 with EGFR mutations and 17 with KRAS mutations. Results: Among 4524 patients with NSCLC tested, NRAS mutations were present in 29 (0.64%). The types of substitutions found were Q61H/K/L/R and G12A/C/D/R/S, with NRAS Q61L the most common (n=14; 48%). One tumor had a concurrent KRAS mutation. 83% had adenocarcinoma histology, with no significant differences in gender. While 90% of patients were former or current smokers, smoking-related G:C>T:A transversions were significantly less frequent in NRAS than in KRAS-mutant NSCLC (KRAS: 66%, NRAS: 13%, p<0.05). Systemic chemotherapy showed limited efficacy in 7 patients with metastatic disease (median OS 7 mos). 5 of 6 NRAS mutant lung cancer cell lines were sensitive to the MEK inhibitors, AZD6244 and GSK1120212, while other targeted agents (against EGFR, ALK, MET, IGF-1R, PIK3CA, BRAF) were minimally effective. Gene expression profiles of NRAS mutant cell lines were distinct from those with KRAS or EGFR mutations. Conclusions: NRAS mutations define a distinct subset of NSCLCs (~1%) with potential sensitivity to MEK inhibitors. While NRAS gene mutations are more common in current/former smokers, the types of mutations are not those classically associated with smoking.

scholarly journals Gene expression profiles of some prognostic markers in a human breast cell line (MCF7) exposed to Curcumin nanoparticles and nanocapsules

2022 ◽  
Author(s):  
Emad Shaker ◽  
Ghada M. Nasr ◽  
Mahmoud Moawad
Keyword(s):  
Breast Cancer ◽  
Mrna Expression ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Prognostic Markers ◽  
Expression Profiles ◽  
Public Health Problem ◽  
Breast Cancer Cell Lines ◽  
Curcumin Nanoparticles

Introduction: Worldwide, cancer is a significant public health problem. Curcumin exhibits anti-inflammatory, antiproliferative, and anticancer properties when used in medicine. Investigated study for Curcumin's chemopreventive mechanism against human malignancies, this research examined the cellular and molecular alterations generated by curcumin modified compound in breast cancer (MCF-7) cell lines. Oncogenic EGFR and VEGFR2 mutations lead to the formation, invasion, and maintenance of malignant phenotypes in humans, including breast cancer. Studied prognostic markers such as C-myc and Ki67 in breast cancer, and the apoptotic gene as Caspase-3 have been done. Aim of the work: The purpose of this study is to determine the therapeutic efficacy of curcumin nanoparticles and nanocapsules in breast cancer cell lines (MCF7). Materials and methods: We used real-time PCR to assess the expression of the C-myc, Ki67, EGFR, VEGFR2, and Caspase-3 genes in MCF7 cells treated with Curcumin nanoparticles and nanocapsules. Results: Curcumin nanoparticles and nanocapsules boosted apoptotic cell populations considerably regardless of the nanotechnology used. Additionally, the mRNA expression analysis results indicated that the mechanism activated by curcumin nanocapsules involved the upregulation of the oncogenes EGFR and VEGFR2. In comparison to curcumin nanoparticles, curcumin nanocapsules significantly reduced the expression of Ki67 and c-myc mRNAs in breast cancer cells. The mRNA expression study revealed that curcumin nanocapsules produce an increase in the apoptotic Caspase-3 gene production compared to cells treated with curcumin nanoparticles. Conclusion: This work demonstrates that curcumin nanoparticles created using a novel mechanical process can be employed successfully as an anticancer agent. These findings add to our understanding of the molecular mechanisms behind curcumin nanocapsules' anticancer activity in breast cancer.

scholarly journals Silencing of the lncRNA H19 enhances sensitivity to X-ray and carbon-ions through the miR-130a-3p /WNK3 signaling axis in NSCLC cells

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xueshan Zhao ◽  
Xiaodong Jin ◽  
Qiuning Zhang ◽  
Ruifeng Liu ◽  
Hongtao Luo ◽  
...  
Keyword(s):  
Cell Lines ◽  
Therapeutic Target ◽  
Ion Irradiation ◽  
Expression Profiles ◽  
Expression Patterns ◽  
Nsclc Cell ◽  
Luciferase Reporter ◽  
Antitumor Effects ◽  
Carbon Ion ◽  
X Ray

Abstract Background The lncRNA H19 is believed to act as an oncogene in various types of tumors and is considered to be a therapeutic target and diagnostic marker. However, the role of the lncRNA H19 in regulating the radiosensitivity of non-small cell lung cancer (NSCLC) cells is unknown. Methods The expression profiles of lncRNAs in NSCLC were explored via transcriptome sequencing. CCK-8, EdU incorporation and clonogenic survival assays were conducted to evaluate the proliferation and radiosensitivity of NSCLC cells. Flow cytometry and Western blotting were conducted to measure the level of apoptosis. The binding relationship between the lncRNA H19 and miR-130a-3p was determined by a dual-luciferase reporter assay. A binding relationship was also identified between miR-130a-3p and With-No-Lysine Kinase 3 (WNK3). Results Expression patterns of lncRNAs revealed that the lncRNA H19 was upregulated in radioresistant NSCLC (A549-R11) cells compared with A549 cells. Knockdown of the lncRNA H19 enhanced the sensitivity of NSCLC cell lines to X-ray and carbon ion irradiation. Mechanistically, the lncRNA H19 serves as a sponge of miR-130a-3p, which downregulates WNK3 expression. The lncRNA H19–miR-130a-3p–WNK3 axis modulates radiosensitivity by regulating apoptosis in NSCLC cell lines. Conclusion Knockdown of the lncRNA H19 promotes the sensitivity of NSCLC cells to X-ray and carbon ion irradiation. Hence, the lncRNA H19 might function as a potential therapeutic target that enhances the antitumor effects of radiotherapy in NSCLC.

Sign in / Sign up

Export Citation Format

Share Document