Pyrvinium Pamoate Induces Cell Apoptosis and Autophagy in Colorectal Cancer.

Background/aim: In earlier research, we demonstrated that pyrvinium pamoate (PP) can effectively inhibit the proliferation and migration of colorectal cancer (CRC) cells. In the current study, we further explore the possibility of PP, as a potential therapeutic drug in the treatment of CRC.

Materials And Methods: Hoechst 33258 staining, immunofluorescence, and western blotting were used to further investigate the connection between PP and CRC cell apoptosis and autophagy.

BMAL1 promotes colorectal cancer cell migration and invasion through ERK- and JNK-dependent c-Myc expression.

Background: Cancer metastasis is still a life threat to patients with colorectal cancer (CRC). Brain and muscle ARNT-like protein 1 (BMAL1) is an important biological proteins that can regulate the behavior of cancer cells and their response to chemotherapy. However, the role of BMAL1 in the tumorigenic phenotype of CRC remains unclear.

Comparative genomic signatures in young and old Chinese patients with colorectal cancer.

Background: Occurrence at a young age is known to be associated with unique clinical features in colorectal cancer (CRC). However, the genomic differences between young and old patients with CRC are not well elucidated and, to the best of our knowledge, have never been investigated in a Chinese population.

Methods: Tumor tissue samples from 29 young (age ≤50 years) and 46 old (age >50 years) patients with CRC were collected.

Pyrvinium pamoate inhibits cell proliferation through ROS-mediated AKT-dependent signaling pathway in colorectal cancer.

The use of the anthelmintic drug pyrvinium pamoate (PP) in cancer therapy has been extensively investigated in the last decade. PP has been shown to have an inhibitory effect in colorectal cancer (CRC), but the underlying mechanism remains elusive. We aimed to investigate the antitumor activity and mechanisms of PP in CRC.

Small molecule 2,3-DCPE induces S phase arrest by activating the ATM/ATR-Chk1-Cdc25A signaling pathway in DLD-1 colon cancer cells.

In our previous study, it was reported that 2[[3-(2,3-dichlorophenoxy)propyl]amino]ethanol (2,3-DCPE) induces apoptosis and cell cycle arrest. The current study aimed to investigate the molecular mechanism involved in 2,3-DCPE-induced S phase arrest. The results demonstrated that 2,3-DCPE upregulated phosphorylated (p-)H2A histone family member X, a biomarker of DNA damage, in the DLD-1 colon cancer cell line.