Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA377341 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5297810_1.fastq.gz | Fastqsanger.gz | |||
| SRR5297810_2.fastq.gz | Fastqsanger.gz | |||
| SRR5297820_1.fastq.gz | Fastqsanger.gz | |||
| SRR5297820_2.fastq.gz | Fastqsanger.gz | |||
| SRR5297801_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 48 |
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Project description:Squamous cell lung carcinoma (SCC) corresponds to about 25% of all lung cancers. Therapeutic approaches are very limited and platinum-based chemotherapy remains the main treatment option. Despite multiple studies, there are no generally accepted predictive biomarkers for SCC. Transforming growth factor-β (TGFβ) signaling was shown to be implicated in numerous pro-tumorigenic processes, including immune evasion, inflammation and cancer metastasis. In the context of SCC epithelial-to-mesenchymal transition phenotype that is commonly mediated by TGFβ was widely observed in surgically resected specimens. However, the relation between TGFβ-induced changes and SCC progression remains to be elucidated. In the presented work, we combined phenotypic and transcriptome-wide approaches to identify novel predictive biomarkers for SCC. We show that TGFβ treatment activated Smad-mediated signal transduction and resulted in increase of migratory and invasive properties of SK-MES1 cells. Multiple actin cytoskeleton-related proteins, including myosin motor proteins such as Myosin-X, were up-regulated upon TGFβ stimulation. siRNA-mediated knockdown of Myosin-X completely abrogated TGFβ-induced collagen gel invasion. Finally, analysis of mRNA expression in paired surgically resected tissues of 151 SCC patients with corresponding 80-month clinical follow-up, showed that the mRNA expression ratio of Myosin-X in tumor and adjacent non-tumor tissue is predictive for overall survival and chemotherapy resistance independently of tumor stage. Given Myosin-X role in cellular motility and invasion, it can represent a new biomarker for aggressive disease and serve as a potential molecular target for therapeutic intervention in patients with SCC.
2018-06-15 | GSE95536 | GEO
Project description:The paper describes a model of resistance of cancer to chemotherapy.
Created by COPASI 4.25 (Build 207)
This model is described in the article:
Modelling chemotherapy resistance in palliation and failed cure
Helen C. Monro, Eamonn A. Gaffney
J Theor Biol. 2009, 257 (2), pp.292
Abstract:
The goal of palliative cancer chemotherapy treatment is to prolong survival and improve quality of life when tumour eradication is not feasible. Chemotherapy protocol design is considered in this context using a simple, robust, model of advanced tumour growth with Gompertzian dynamics, taking into account the effects of drug resistance. It is predicted that reduced chemotherapy protocols can readily lead to improved survival times due to the effects of competition between resistant and sensitive tumour cells. Very early palliation is also predicted to quickly yield near total tumour resistance and thus decrease survival duration. Finally, our simulations indicate that failed curative attempts using dose densification, a common protocol escalation strategy, can reduce survival times.
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2024-09-02 | BIOMD0000000776 | BioModels
Project description:Standard chemotherapy for lung cancer often leads to drug resistance, posing a significant clinical challenge. A major mechanism of resistance is overexpression of P-glycoprotein (P-gp), encoded by the human ATP-binding cassette subfamily B member 1 (hABCB1) gene, functioning as a drug efflux transporter. In this study, we aimed to investigate the dual role of hABCB1 overexpression in mediating resistance to chemotherapy and natural killer (NK) cell-mediated cytotoxicity in lung cancer.
2025-01-06 | MSV000096780 | MassIVE
Project description:Lung cancer is the leading cause of cancer mortality and is classified by the World Health Organization into two broad histological subtypes. Non–small cell lung cancer (NSCLC), including adenocarcinoma, squamous cell carcinoma, and large cell carcinoma, accounts for ~85% of all lung cancer cases, with the remaining 15% of cases being due to small cell lung cancer (SCLC), which arises from neuroendocrine cells in the lung. Although most SCLC tumors are initially responsive to chemotherapy and radiation, patients often experience relapse, with the tumor acquiring an aggressiveness and therapeutic resistance that lead to a poor clinical outcome. Improvement of overall survival in individuals with SCLC will require the identification of novel therapeutic targets based on a better understanding of the changes in intracellular signaling of aggressive SCLC cells. The malignant progression of SCLC often occurs concomitantly with the acquisition of chemoresistance, suggesting that phenotypic malignant change is related to adaptation to the stresses induced by chemotherapy. In order to analyze gene expression changes associated with malignant transformation in SCLC, we established a cisplatin-resistant SCLC cell line and performed RNA sequencing.
2021-03-04 | GSE168184 | GEO
Project description:Lung cancer is the leading cause of cancer mortality and is classified by the World Health Organization into two broad histological subtypes. Non–small cell lung cancer (NSCLC), including adenocarcinoma, squamous cell carcinoma, and large cell carcinoma, accounts for ~85% of all lung cancer cases, with the remaining 15% of cases being due to small cell lung cancer (SCLC), which arises from neuroendocrine cells in the lung. Although most SCLC tumors are initially responsive to chemotherapy and radiation, patients often experience relapse, with the tumor acquiring an aggressiveness and therapeutic resistance that lead to a poor clinical outcome. Improvement of overall survival in individuals with SCLC will require the identification of novel therapeutic targets based on a better understanding of the changes in intracellular signaling of aggressive SCLC cells. The malignant progression of SCLC often occurs concomitantly with the acquisition of chemoresistance, suggesting that phenotypic malignant change is related to adaptation to the stresses induced by chemotherapy. In order to analyze gene expression changes associated with malignant transformation in SCLC, we established a cisplatin-resistant SCLC cell line and performed RNA sequencing.
2025-03-31 | GSE280212 | GEO
Project description:Chemotherapy resistance adversely impacts the treatment of some individuals with esophageal cancer. Identifying chemotherapy resistance might help tailor clinical treatments. In this study the impact of microRNAs on chemotherapy resistance in esophageal cancer was investigated. We used microarrays to detail the global programme of microRNA expression underlying chemotherapy resistance and identified distinct classes of up-regulated microRNAs in generated chemotherapy resistant cell lines. An in-vitro model of acquired chemotherapy resistance in esophageal adeno- (EAC) and squamous cell carcinoma (SCC) cells was used, and microRNA expression profiles for cisplatin or 5-fluorouracil (FU) resistant variants vs. chemotherapy sensitive controls were compared using microarray. These results were further validated using qRT-PCR techniques (not shown in this submission).
2013-08-28 | E-GEOD-50224 | biostudies-arrayexpress
Project description:KIAA1522 is aberrantly over-expressed and predicts the outcome of platinum-base chemotherapy. Down-regulation of KIAA1522 sensitizes lung adenocarcinoma cells to cisplatin. To evaluate the molecular mechanisms underlying KIAA1522-induced cisplatin resistance. The RNA sequencing assays were performed in KIAA1522-depleted 889 cells.
2020-08-31 | GSE146072 | GEO
Project description:The higher immunogenicity of tumors usually predicts favorable therapeutic responses. Tumor antigens dominate the immunogenic character within tumors. We investigated if there was a targetable tumor antigen during immunogenic chemotherapy within lung cancer. Chemotherapy-induced immunogenic senescence was demonstrated using a multi-marker, three-step workflow and RNA-sequencing data. The ability of anti-lung-specific X protein (LUNX) antibody to suppress the survival of senescent lung cancer cells was evaluated in vitro and in vivo using real-time cytotoxicity analysis and xenograft mouse models, respectively. The induction of cellular senescence by immunogenic chemotherapy boosted cell-surface shuttling of LUNX and enhanced the immunogenic features of senescent tumor cells, which sensitized lung cancer cells to anti-LUNX antibody-mediated therapy and contributed to tumor suppression. The immunogenic senescence-mediated anti-tumor response was triggered by the direct action of antibody on tumor cells, strengthened by natural-killer cells through an antibody-dependent cell-mediated cytotoxicity response and, ultimately, led to tumor control. Our findings suggest that LUNX is a lung cancer targetable-immunogenic antigen. The proportion of lung cancers responding to LUNX-targeting therapy could be expanded substantially by immunogenic chemotherapy that induces senescence-associated translocation of LUNX to the plasma membrane.
2024-10-03 | GSE185208 | GEO
Project description:The higher immunogenicity of tumors usually predicts favorable therapeutic responses. Tumor antigens dominate the immunogenic character within tumors. We investigated if there was a targetable tumor antigen during immunogenic chemotherapy within lung cancer. Chemotherapy-induced immunogenic senescence was demonstrated using a multi-marker, three-step workflow and RNA-sequencing data. The ability of anti-lung-specific X protein (LUNX) antibody to suppress the survival of senescent lung cancer cells was evaluated in vitro and in vivo using real-time cytotoxicity analysis and xenograft mouse models, respectively. The induction of cellular senescence by immunogenic chemotherapy boosted cell-surface shuttling of LUNX and enhanced the immunogenic features of senescent tumor cells, which sensitized lung cancer cells to anti-LUNX antibody-mediated therapy and contributed to tumor suppression. The immunogenic senescence-mediated anti-tumor response was triggered by the direct action of antibody on tumor cells, strengthened by natural-killer cells through an antibody-dependent cell-mediated cytotoxicity response and, ultimately, led to tumor control. Our findings suggest that LUNX is a lung cancer targetable-immunogenic antigen. The proportion of lung cancers responding to LUNX-targeting therapy could be expanded substantially by immunogenic chemotherapy that induces senescence-associated translocation of LUNX to the plasma membrane.
2024-10-03 | GSE185207 | GEO
Project description:In this study, we have analyzed the transcriptional patterns of breast cancer cell lines and tumors of NAC resistant patients evaluated by GGI, and screened potential genes associated with chemoresistance. Furthermore, we have constructed a neoadjuvant chemotherapy response risk model and examined the evaluation accuracy of the risk score for NAC response. We conducted molecular bioinformatics analysis of the genes that constitute the chemotherapy resistance risk score, and explored potential drugs to reverse breast cancer chemotherapy resistance. Finally, we have examined the the risk score for predicting prognosis in breast cancer. In all, we have reported a novel signature to evaluate neoadjuvant chemotherapy response and predicts prognosis in breast cancer, and screened out potential drugs to reverse chemotherapy resistance in breast cancer.
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