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Identification of genes involved in enhancement of hyperthermia sensitivity by knockdown of BAG3 in human oral squamous cell carcinoma cells

ABSTRACT: Hyperthermia (HT) treatments in combination with either chemotherapy, radiotherapy or both are used for patients with cancer in various organs. However, the acquisition of thermotolerance in cancer cells due to the increase in cytoprotective proteins attenuates the therapeutic effects of HT. BAG3 (BCL2-associated athanogene 3) is a cytoprotective protein that acts against various stresses including heat stress. Recently, we demonstrated that the inhibition of BAG3 improves cell death sensitivity to HT in cancer cells. However, a detailed molecular mechanism involved in the enhancement of HT sensitivity by BAG3-knockdown (KD) in cancer cells is unclear. In this study, to identify genes involved in the enhancement of HT sensitivity by BAG3-knockdown (KD) in cancer cells, global-scale gene expression analysis was carried out using a GeneChipÂ® system. Human oral squamous carcinoma cell HSC-3 cells were treated with a combination of HT (at 44Â°C for 90 min) and siRNA for BAG3 or luciferase. Total RNA samples were prepared from the cells, and quality of the RNA was analyzed using a Bioanalyzer 2100. Gene expression was analyzed by an Affymetrix GeneChipÂ® system with a Human Genome U133-plus 2.0 array. Sample preparation for array hybridization was carried out as described in the manufacturerâs instructions.

ORGANISM(S): Homo sapiens

SUBMITTER: Yoshiaki Tabuchi

PROVIDER: E-GEOD-75127 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Identification of genes involved in enhancement of hyperthermia sensitivity by knockdown of BAG3 in human oral squamous cell carcinoma cells

Project description:Hyperthermia (HT) treatments in combination with either chemotherapy, radiotherapy or both are used for patients with cancer in various organs. However, the acquisition of thermotolerance in cancer cells due to the increase in cytoprotective proteins attenuates the therapeutic effects of HT. BAG3 (BCL2-associated athanogene 3) is a cytoprotective protein that acts against various stresses including heat stress. Recently, we demonstrated that the inhibition of BAG3 improves cell death sensitivity to HT in cancer cells. However, a detailed molecular mechanism involved in the enhancement of HT sensitivity by BAG3-knockdown (KD) in cancer cells is unclear. In this study, to identify genes involved in the enhancement of HT sensitivity by BAG3-knockdown (KD) in cancer cells, global-scale gene expression analysis was carried out using a GeneChip® system.

2015-11-19 | GSE75127 | GEO

Identification of genes responsive to mild hyperthermia in human oral squamous cell carcinoma HSC-3 cells

Project description:Hyperthermia (HT) is widely used to treat patients with various cancers. In general, HT elicits a wide spectrum of stress responses, such as induction of heat shock proteins, protein aggregation and cell death in mammalian cells. Although many biological processes are affected by HT, the overall responses to HT in mammalian cells remain unknown. The effects of heat stress at 41Â°C for 30 min (mild hyperthermia) on the gene expression in human oral squamous cell carcinoma HSC-3 cells were investigated using an Affymetrix GeneChip system. Human oral squamous cell carcinoma HSC-3 cells were treated with heat stress (41Â°C for 30 min), followed by incubation for 0, 1, or 3 h at 37Â°C. Non-treated cells served as control. Total RNA samples were prepared from the cells, and quality of the RNA was analyzed using a Bioanalyzer 2100. Gene expression was monitored by an Affymetrix GeneChipÂ® system with a Human Genome U133-Plus 2.0 array. Sample preparation for array hybridization was carried out as described in the manufacturer's instructions.

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The pancreatic cancer stem cell marker CD44v6 affects transcription, translation and signaling: consequences on exosome composition and delivery II

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microRNA expression profile from five Ehlers-Danlos Syndrome Hypermobility type/Joint Hypermobility Syndrome (EDS-HT/JHS) patients' skin fibroblasts

Project description:To screen for potential miRNA that may contribute to the etiopathogenesis of EDS-HT/JHS miRNA expression profiling was performed using the Affymetrix GeneChipÂ® miRNA 3.0 Array and comparing the miRNA expression changes of skin fibroblasts of five EDS-HT/JHS patients with those of six healthy individuals Comparison of miRNA expression profiles between five EDS-HT/JHS human fibroblasts and six controls

2016-08-05 | E-GEOD-77756 | biostudies-arrayexpress

The pancreatic cancer stem cell marker CD44v6 affects transcription, translation and signaling: consequences on exosome composition and delivery I

2018-08-25 | GSE119031 | GEO

The pancreatic cancer stem cell marker CD44v6 affects transcription, translation and signaling: consequences on exosome composition and delivery III

Project description:The miRNA profile between EXO from different pancreatic adenocarcinoma cells (A818.4, Capan-1) and different colorectal carcinoma cells (SW948, HT-29). The impact of a knockdown (kd) of function-relevant cancer stem cell markers (CD44v6, Tspan8, CD151, claudin7) on the EXO miRNA profile. The EXO kd cell miRNA profiles were compared with the wt cell EXO as well as between the different kd EXO miRNA profiles. These analyses were important to elaborate joint miRNA in the EXO profile from different cell lines as a starting point to elaborate possible functional activities of EXO including therapeutic translation.

2018-08-25 | GSE119033 | GEO

Spontaneous metastasis xenograft models link CD44 isoform 4 to angiogenesis, hypoxia, EMT and mitochondria-related pathways in colorectal cancer

Project description:Objective: To determine the functional relevance of CD44 isoforms for distant metastasis formation in human colorectal cancer (CRC). Design: We used a pan-CD44 knockdown (kd) approach in a clinically relevant cell line/ xenograft model (HT-29) that spontaneously metastasizes to multiple sites in vivo. Transcriptomics, proteomics and kinomics were used in addition to corresponding validation steps to explain the observed effects. Findings were further corroborated by 3D in vitro culture, tissue microarray and bioinformatics analyses. Results: HT-29 cells mainly express the clinically relevant CD44 isoforms 3 and 4. CD44 kd impairs primary tumor formation and abrogates distant metastasis in vivo. Both CD44 isoforms are induced in the paranecrotic, hypoxic regions of the xenograft primary tumors but are largely absent in the corresponding lung metastases. Tumor angiogenesis is improved in the paranecrosis upon CD44 kd, accompanied by reduced HIF-1α, EMT, and CEACAM5 expression. Vice versa, mitochondrial genes and proteins are induced upon CD44 kd as is oxidative phosphorylation. Hypoxia increases VEGF release from 3D HT-29 spheres, which is strikingly enhanced in CD44 kd spheres. The metastasis-promoting role of CD44 is reflected by an unfavorable prognostic effect of CD44 isoform 4 in patients (as opposed to isoform 3). Accordingly, the genes regulated by the CD44 kd in vivo concordantly overlap specifically with the genes regulated by CD44 isoform 4 in patients. Conclusion: In CRC, CD44 kd (most probably isoform 4) evidently impairs metastasis formation by improving VEGF release and thus angiogenesis in hypoxic conditions, thereby decreasing hypoxia, EMT, stemness, and promoting mitochondrial metabolism.

2022-07-18 | GSE208310 | GEO

Therapeutic potential for reversing miR-634-mediated cytoprotective processes to improve the efficacy of chemotherapy against oral squamous cell carcinoma

Project description:For advanced oral squamous cell carcinoma (OSCC), increasing sensitivity to chemotherapy is a major challenge in improving treatment outcomes, and targeting cytoprotective processes that lead to the chemotherapy resistance of cancer cells may be therapeutically promising. Tumor-suppressive microRNAs (miRs) can target multiple cancer-promoting genes concurrently, and are thus expected to be useful seeds for cancer therapeutics. We revealed that miR-634-meditated targeting of multiple cytoprotective process-related genes, including cellular inhibitor of apoptosis proteins 1 (cIAP1), can effectively increase cisplatin (CDDP)-induced cytotoxicity and overcome CDDP resistance in OSCC cells. The combination of topical treatment with miR-634 ointment and administration of CDDP was synergistically effective against OSCC-tumor growth in a xenograft mouse model. Furthermore, the expression of miR-634 target genes is frequently upregulated in primary OSCC tumors. Our study suggests that reversing miR-634-mediated cytoprotective processes activated in cancer cells is a potentially useful strategy to improve CDDP efficacy against advanced OSCC.

2022-05-25 | GSE194269 | GEO

LncRNA and mRNA expression profiling reveals the molecular mechanism of hyperthermia sensitizing human gastric cancer cisplatin- resistant cell line SGC-7901/DDP

Project description:Gastric cancer (GC) is the second leading cause of cancer-related death in the world, but due to the emergence of drug resistance, the chemotherapy effect of GC has not been improved. Hyperthermia (HT) can increase the sensitivity of tumor cells to chemotherapeutic drugs and cause the specific expression of related genes. Therefore, we want to confirm that HT can enhance the sensitivity of SGC-7901/DDP cells to cisplatin (DDP) and explore the molecular mechanism of sensitization. To study the optimal experimental conditions with synergistic effect, temperature gradients (41 ℃, 44 ℃, 47 ℃, 50 ℃), time gradients (12 h, 24 h, 36 h) and DDP concentration gradients (1 μg/ml, 2 μg/ml, 3 μg/ml) were established. Then the microarray analysis was performed to explore the molecular mechanism of HT sensitization. Our results showed that 47 ℃ HT+ 2 μg/ml DDP for 24 h could synergistically inhibit the proliferation of SGC7901/DDP cells and significantly promote early apoptosis. Differentially expressed lncRNAs and mRNAs between groups were obtained. ENST00000434470.1(IDI2-AS1), ENST00000592689.1(TTN-AS1) and ENST00000412526.1(LINC00161) may play a pro-apoptotic role, while asRNAs could be a potential target for the treatment of GC. KEGG pathway enrichment showed that DDP+HT may induce apoptosis of SGC7901/DDP cells through GPCR signaling pathway, BARD signaling pathway and TRAIL signaling pathway. In summary, HT can enhance the sensitivity of SGC-7901/DDP cells to DDP by activating related apoptotic genes and pathways.

2021-04-01 | GSE147385 | GEO

MetaboLights MTBLS1066 - GNPS Untargeted Metabolomics Reveals Molecular Effects of Ketogenic Diet on Healthy and Tumor Xenograft Mouse Models.

Project description:The application of ketogenic diet (KD) (high fat/low carbohydrate/adequate protein) as an auxiliary cancer therapy is a field of growing attention. KD provides sufficient energy supply for healthy cells, while possibly impairing energy production in highly glycolytic tumor cells. Moreover, KD regulates insulin and tumor related growth factors (like insulin growth factor-1, IGF-1). In order to provide molecular evidence for the proposed additional inhibition of tumor growth when combining chemotherapy with KD, we applied untargeted quantitative metabolome analysis on a spontaneous breast cancer xenograft mouse model, using MDA-MB-468 cells. Healthy mice and mice bearing breast cancer xenografts and receiving cyclophosphamide chemotherapy were compared after treatment with control diet and KD. Metabolomic profiling was performed on plasma samples, applying high-performance liquid chromatography coupled to tandem mass spectrometry. Statistical analysis revealed metabolic fingerprints comprising numerous significantly regulated features in the group of mice bearing breast cancer. This fingerprint disappeared after treatment with KD, resulting in recovery to the metabolic status observed in healthy mice receiving control diet. Moreover, amino acid metabolism as well as fatty acid transport were found to be affected by both the tumor and the applied KD. Our results provide clear evidence of a significant molecular effect of adjuvant KD in the context of tumor growth inhibition and suggest additional mechanisms of tumor suppression beyond the proposed constrain in energy supply of tumor cells.

2020-08-01 | MSV000085879 | GNPS

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