We examined the effects of troglitazone on expression of E-cadherin and claudin 4 in human pancreatic cancer cells. Troglitazone dose-dependently increased expression of E-cadherin and claudin 4 mRNA and protein in PK-1 cells. Snail, Slug and ZEB1, mRNAs were not changed by troglitazone, indicating that these three transcriptional repressors would not play a role in the induction of E-cadherin by troglitazone. GW9662, a PPARgamma antagonist, failed to block the increased expression of E-cadherin or claudin 4 mRNA, suggesting a PPARgamma-independent pathway. A MEK inhibitor, U0126, increased E-cadherin or claudin 4 mRNA and protein expression, and potently inhibited cell invasion. Because troglitazone down-regulates MEK-ERK signaling and inhibit cell invasion in PK-1 as shown in our previous study, these results suggest that troglitazone increases expression of E-cadherin and claudin 4 possibly through inhibition of MEK-ERK signaling in pancreatic cancer cells, which might be involved in the troglitazone-induced inhibition of cell invasive activity.
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http://dx.doi.org/10.1016/j.bbrc.2009.01.134 | DOI Listing |
Eur J Histochem
January 2025
Department of Critical Care Medicine, The Qujing No.1 People's Hospital, Qujing.
Intestinal barrier damage causes an imbalance in the intestinal flora and microbial environment, promoting a variety of gastrointestinal diseases. This study aimed to explore the mechanism by which adipose-derived stem cells (ADSCs) repair intestinal barrier damage. The human colon adenocarcinoma cell line Caco-2 and rats were treated with lipopolysaccharide (LPS) to establish in vitro and in vivo models, respectively, of intestinal barrier damage.
View Article and Find Full Text PDFJ Ethnopharmacol
January 2025
School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China. Electronic address:
Ethnopharmacological Relevance: Huanglian Ganjiang decoction (HGD), which is composed of Chinese medicines with cold, warm, and astringent properties, has demonstrated significant therapeutic efficacy in ulcerative colitis (UC). However, the underlying mechanisms remain unclear, highlighting the need for a multi-faceted investigation. Disassembling prescriptions is a crucial approach for investigating compatibility mechanisms.
View Article and Find Full Text PDFJ Ethnopharmacol
January 2025
The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, 210023, China. Electronic address:
Gene
February 2025
All India Institute of Medical Sciences (AIIMS), Mangalagiri, Andhra Pradesh, India.
Background And Aims: MicroRNAs (miRNAs) are becoming progressively emerging in cancer research from an etiologic and curative point of view. Several miRNAs act as oncogenes or tumor suppressors, which are dysregulated in numerous cancers. Our previous studies have established that nimbolide (a bioactive terpenoid from neem) attenuated hepatocellular carcinoma (HCC) through various mechanisms in mice.
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
November 2024
School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou 510006, China.
Objective: To evaluate the therapeutic effect of Decoction (HQD) on ulcerative colitis (UC) in mice and explore its mechanism.
Methods: Male Balb/c mice were randomly divided into normal control group, model group, mesalazine group (5-ASA, 200 mg/kg), and low-, medium-and high-dose HQD groups (2.275, 4.
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