RUI ZHANG^1,2,#, PENG ZHOU^1,3,#, XIA OU⁴, PEIZHU ZHAO², XIJING GUO², MIAN XI^5,*, CHEN QING^1,*

Oncology Research, Vol.31, No.6, pp. 887-897, 2023, DOI:10.32604/or.2023.030184

Abstract Esophageal squamous cell carcinoma (ESCC) is among the most prevalent causes of cancer-related death in patients worldwide. Resistance to immunotherapy and chemotherapy results in worse survival outcomes in ESCC. It is urgent to explore the underlying molecular mechanism of immune evasion and chemoresistance in ESCC. Here, we conducted RNA-sequencing analysis in ten ESCC tissues from cisplatin-based neoadjuvant chemotherapy patients. We found that DMRTA1 was extremely upregulated in the non-pathologic complete response (non-pCR) group. The proliferation rate of esophageal squamous carcinoma cells was markedly decreased after knockdown of DMRTA1 expression, which could increase cisplatin sensitivity in ESCC. Additionally, suppression of DMRTA1… More >

ISIDORA PETROVIC¹, MILENA MILIVOJEVIC¹, ANA ARSENIJEVIC², ANDRIJANA LAZIC¹, NATASA KOVACEVIC GRUJICIC¹, MARIJA SCHWIRTLICH¹, JELENA POPOVIC³, MILENA STEVANOVIC^1,4,5,*

BIOCELL, Vol.45, No.5, pp. 1355-1367, 2021, DOI:10.32604/biocell.2021.015817

Abstract Genetic and molecular heterogeneity, together with intrinsic and acquired resistance to therapy, represent the major obstacles to the successful treatment of different types of breast carcinoma. Increasing evidence demonstrates that SOX transcription factors in breast carcinomas could act both as oncogenes and tumor suppressors and have been associated with tumor stage and grade, poor prognosis, and therapy resistance. Both SOX2 and SOX18 overexpression has been correlated with poor prognosis in breast carcinomas, and these genes are recognized as potential antitumor targets. Our aim was to evaluate the effect of retinoic acid (RA), a well-known cyto-differentiating agent, on breast carcinoma cells… More >

HAIFENG WANG^1,2, KAI WANG¹, JUAN GUO¹, TIEQIAO WEN²

BIOCELL, Vol.43, No.2, pp. 59-64, 2019, DOI:10.32604/biocell.2019.05731

Abstract Histone deacetylation is a key modulator involved in cell proliferation, apoptosis, and mRNA transcription. However, the effects of histone deacetylation on C17.2 neural stem cells (NSCs) remain unclear. Here, the histone deacetylase inhibitors nicotinamide and trichostatin A (TSA) were used to determine the role of histone deacetylation on gene transcription in NSCs. The results showed that the mRNA expression of p53, Sox1, Sox2, and Bax were significantly higher in E14.5 NSCs than in C17.2 NSCs. Nestin, a marker gene of neuronal differentiation, did not differ significantly between E14.5 NSCs and C17.2 NSCs. The transcription levels of p53 and Nestin were… More >