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The study of the effects of dauricine(dau) on human pancreatic carcinoma cells [mRNA array]

ABSTRACT: Pancreatic cancer is one of the most malignant digestive tract tumors with the worst prognosis. Few treatments are available; thus, the discovery of potential new anti-cancer agents has always been a hot issue. Dauricine (Dau) can inhibit the proliferation of the pancreatic cancer cell line BxPC3, and has the potential to be used as an adjuvant drug against pancreatic cancer; however, how Dau inhibits tumor cell proliferation has not been elucidated. To unravel the effects of Dau on proteins and metabolic pathways of pancreatic cancer cells, and to elucidate its anticancer mechanisms, we evaluated mRNA and microRNA expression in BxPC3 cells treated with Dau.

ORGANISM(S): Homo sapiens

PROVIDER: GSE176162 | GEO | 2021/06/05

REPOSITORIES: GEO

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Project description:Purpose: Chemotherapy is pivotal in the multimodal treatment of pancreatic cancer patients. In recent years, technical advances have developed experimental methods that unveiled a high degree of inter- and intratumoral heterogeneity in pancreatic cancer. We hypothesized that intratumoral heterogeneity (ITH) impacts response to gemcitabine treatment and demands specific targeting of resistant subclones. Experimental Design: We addressed the effect of ITH on response to gemcitabine treatment using single cell-derived cell lines (SCDCL) from the classical-like cell line BxPC3 and the basal-like cell line Panc-1 which were analyzed by mRNA-seq and mass spectrometry. Results: Individual SCDCLs of the parental tumor cell populations of BxPC3 and Panc-1 showed considerable heterogeneity in response to gemcitabine. Unsupervised principal component analysis (PCA) including the 1,000 most variably expressed genes showed a clustering of the SCDCLs according to their respective sensitivity to gemcitabine treatment for BxPC3, while this clustering was less clear for Panc-1. In BxPC3 SCDCLs, enriched signaling pathways EMT, TNF signaling via NfKB, and IL2STAT5 signaling correlated with more resistant behavior to gemcitabine. In Panc-1 SCDCLs MYC targets V1 and V2 as well as E2F targets were associated with stronger resistance to gemcitabine. Feature extraction of proteomes again identified less proteins whose expression was associated with the response of individual SCDCLs in Panc-1 compared to BxPC3. Based on molecular profiles, we could show that the gemcitabine-resistant SCDCLs of both BxPC3 and Panc-1 are more sensitive to the BET inhibitor JQ1 compared to the respective gemcitabine-sensitive SCDCLs. Conclusions: Our model system of SCDCLs identified gemcitabine-resistant subclones within a parental tumor population and provides evidence for the critical role of ITH for treatment response in pancreatic cancer. Through molecular profiling, we identified specific signaling pathways and protein signatures that might help to explain the differential response to treatment among clones. We exploited these molecular differences for an improved and more targeted therapy of resistant subclones of a heterogeneous tumor.

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The study of the effects of dauricine(dau) on human pancreatic carcinoma cells [mRNA array]

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