4.5 Article

Effective anticancer agents based-on two Pillar[5]arene derivatives for pancreas cancer cell lines: synthesis, apoptotic effect, caspase pathway

Journal

INVESTIGATIONAL NEW DRUGS
Volume 41, Issue 2, Pages 202-209

Publisher

SPRINGER
DOI: 10.1007/s10637-023-01343-w

Keywords

Pancreas cancer; Pillar[5]aren; Panc-1; BxPC-3

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This study aimed to evaluate the anticancer effects of two different pillar[5]arene derivatives on pancreatic cancer cell lines. Changes in gene expression and apoptosis rate were investigated. The results showed that the pillar[5]arenes upregulated proapoptotic genes and genes involved in major caspase activation, while down-regulating antiapoptotic genes in the Panc-1 cell line. However, the apoptosis pathway was not active in the BxPC-3 cell line.
This study aimed to evaluate the possible anticancer effects of two different pillar[5]arene derivatives (5Q-[P5] and 10Q-P[5]) on two different pancreatic cancer cell lines in vitro. For this purpose, changes in the expression of major genes that play a role in apoptosis and caspase pathways were investigated. Panc-1 and BxPC-3 cell lines were used in the study and the cytotoxic dose of pillar[5]arenes was determined by the MTT method. Changes in gene expression after pillar[5]arenes treatment were evaluated by real-time polymerase chain reaction (qPCR). Apoptosis was studied by flow cytometry. As a result of analysis, it was determined that proapoptotic genes and genes involved in major caspase activation were upregulated and antiapoptotic genes were down-regulated in Panc-1 cell line treated with pillar[5]arenes. Flow cytometric apoptosis analysis also showed an increased apoptosis rate in this cell line. On the contrary, although MTT analysis showed cytotoxic effect in BxPC-3 cell line treated with two pillar[5]arene derivatives, the apoptosis pathway was not active. This suggested that it may activate different death pathways for BxPC-3 cell line. Thus, it was first determined that the pillar[5]arene derivatives reduced cancer cell proliferation on pancreatic cancer cells.

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