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Gene expression analysis of human oral squamous cell carcinoma cell lines (HSC-4, OSC19)

ABSTRACT: As microarray based gene expression profiling is well suited to study the complex diseases such as cancer, we revealed gene expression changes of two different cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE41495 | GEO | 2012/10/12

SECONDARY ACCESSION(S): PRJNA177223

REPOSITORIES: GEO

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Gene expression analysis of human oral squamous cell carcinoma cell lines (HSC-4, OSC19)

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Gene expression analysis of human oral squamous cell carcinoma cell lines (HSC-4, OSC19)

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Podocalyxin is crucial for the growth of oral squamous cell carcinoma cell line HSC-2.

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Gene expression profiling in HSF1-knockdown human oral squamous cell carcinoma HSC-3 cells

Project description:Heat shock transcription factor 1 (HSF1) is recognized as the major regulator of the heat shock transcriptional response, and also plays a central role in the cellular functions of cancer cells. Here, to identify the molecular mechanism by which HSF1 regulates the proliferation of cancer cells, comparative gene expression analysis was performed with mock and HSF1-knockdown cells. Silencing of HSF1 in human oral squamous cell carcinoma HSC-3 cells was carried out by siRNA technology and the expression of HSF1 was confirmed by Western blotting. Gene expression was analyzed using GeneChip oligonucleotide microarrays and computational gene expression analysis tools. HSF1 knockdown significantly decreased the number of viable cells. Of the 54,675 probe sets analyzed, 221 probe sets were up-regulated and 423 probe sets were down-regulated by >2-fold in HSF1-knockdown cells. HSC-3 human oral squamous carcinoma cells were treated with siRNA for HSF1 or luciferase. Total RNA samples were prepared from the cells. Gene expression was analyzed by an Affymetrix GeneChip® 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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Project description:Epidermal growth factor receptor (EGFR) is involved in multiple aspects of cancer cell biology. EGFR has already been identified as an important target for cancer therapy, with various kinds of EGFR inhibitors currently used in treatment of several human cancers. Recently, EGFR and its downstream signaling pathways were identified as being associated with cisplatin sensitivity. In addition, EGFR inhibitors have shown significant promise for patients who failed cisplatin-based therapy. In this study, we investigated whether treatment with an EGFR inhibitor improves cisplatin sensitivity in oral squamous cell carcinoma (OSCC) cell lines. The effects of a combination of AG1478, a specific EGFR tyrosine kinase inhibitor, with cisplatin were evaluated in cultured OSCC cell lines and cisplatin-resistant sublines. Higher expression of EGFR and p-EGFR was found in the two cisplatin-resistant cell lines compared with the corresponding parental cell lines. In addition, augmented inhibition of OSCC cell growth by the combination of AG1478 with cisplatin was found in both cell lines. These results suggest that the combination of an EGFR inhibitor and cisplatin may be useful as a rational strategy for the treatment of patients with oral cancer with acquired cisplatin resistance.

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HIKESHI silencing can enhance mild hyperthermia sensitivity in human oral squamous cell carcinoma HSC‑3 cells.

Project description:Hyperthermia (HT) is considered to be of value as a treatment modality in various cancers. However, the acquisition of thermotolerance in cancer cells due to the induction of heat shock proteins (HSPs) makes HT less effective. Recent findings have indicated that heat shock protein nuclear import factor hikeshi (HIKESHI), also referred to as C11orf73, acts as a nuclear import carrier of Hsp70 under heat stress conditions. The aim of the present study was to determine whether knockdown (KD) of HIKESHI by small interfering RNA (siRNA) can potentiate mild HT (MHT) sensitivity in human oral squamous cell carcinoma (OSCC) HSC‑3 cells. The mRNA and protein expression of HIKESHI was found to be markedly suppressed in HSC‑3 cells treated with siRNA for HIKESHI (siHIKE). Silencing HIKESHI significantly decreased the cell viability under MHT conditions (42˚C for 90 min). Immunocytochemical and western blot analyses clearly demonstrated that Hsp70 protein translocated from the cytoplasm to the nucleus under MHT conditions, and this translocation was significantly inhibited in cells treated with siHIKE. Treatment of the cells with MHT transiently increased the phosphorylation level of extracellular signal‑regulated kinase (ERK)2. Furthermore, the phosphorylation was sustained in HIKESHI‑KD cells under MHT conditions, and this sustained phosphorylation was abolished by pretreatment with U0126, an inhibitor of mitogen‑activated protein kinase/ERK. In addition, U0126 significantly decreased the viability of cells treated with the combination of HIKESHI‑KD and MHT. The data of the present study suggest that HIKESHI silencing enhanced the sensitivity of human OSCC HSC‑3 cells to MHT.

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