FENGXIANG TANG, YANSHI LI, MIN PAN, ZHIHAI WANG, TAO LU, CHUAN LIU, XIN ZHOU, GUOHUA HU^*

Oncology Research, Vol.31, No.5, pp. 787-803, 2023, DOI:10.32604/or.2023.030081

Abstract Background: Lymphatic metastasis (LM) emerges as an independent prognostic marker for hypopharyngeal squamous cell carcinoma (HSPSCC), chiefly contributing to treatment inefficacy. This study aimed to scrutinize the prognostic relevance of HSP90AA1 and its potential regulatory mechanism of concerning LM in HPSCC. Methods: In a preceding investigation, HSP90AA1, a differential gene, was discovered through transcriptome sequencing of HPSCC tissues, considering both the presence and absence of LM. Validation of HSP90AA1 expression was accomplished via qRT-PCR, western-blotting(WB), and immunohistochemistry(IHC), while its prognostic significance was assessed employing Kaplan–Meier survival analysis(KMSA), log-rank test(LR), and Cox’s regression analysis(CRA). Bioinformatics techniques facilitated the prediction and analysis… More > Graphic Abstract

MASANORI KAWANO, KAZUHIRO TANAKA^*, ICHIRO ITONAGA, TATSUYA IWASAKI, YUTA KUBOTA, HIROSHI TSUMURA

Oncology Research, Vol.31, No.5, pp. 631-643, 2023, DOI:10.32604/or.2023.029745

Abstract Heat shock protein (HSP) 90 plays a crucial role in correcting the misfolded three-dimensional structure of proteins, assisting them in folding into proper conformations. HSP90 is critical in maintaining the normal functions of various proteins within cells, as essential factors for cellular homeostasis. Contrastingly, HSP90 simultaneously supports the maturation of cancer-related proteins, including mesenchymal epithelial transition factor (MET) within tumor cells. All osteosarcoma cell lines had elevated MET expression in the cDNA array in our possession. MET, a tyrosine kinase receptor, promotes proliferation and an anti-apoptotic state through the activation of the MET pathway constructed by HSP90. In this study,… More > Graphic Abstract

Hyun-Jung Moon,1 So-Young Park,1 Su-Hoon Lee, Chi-Dug Kang, Sun-Hee Kim

Oncology Research, Vol.27, No.7, pp. 835-847, 2019, DOI:10.3727/096504019X15517850319579

Abstract Recently, novel therapeutic strategies have been designed with the aim of killing cancer stem-like cells (CSCs), and considerable interest has been generated in the development of specific therapies that target stemnessrelated marker of CSCs. In this study, nonsteroidal anti-inflammatory drugs (NSAIDs) significantly potentiated Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG)-mediated cytotoxicity through apoptotic and autophagic cell death induction, but COX-2-inhibitory function was not required for NSAIDinduced autophagy in CD44-overexpressing human chronic myeloid leukemia K562 (CD44^highK562) cells. Importantly, we found that treatment with NSAIDs resulted in a dose-dependent increase in LC3-II level and decrease in p62 level and simultaneous reduction in multiple stemness-related markers… More >