Tyrosine phosphatase SHP2 promoted the progression of CRC via modulating the PI3K/BRD4/TFEB signaling induced ferroptosis.

Objective: To elucidate the mechanism by which tyrosine phosphatase SHP2 protects CRC through modulation of TFEB-mediated ferritinophagy, thereby suppressing ROS and ferroptosis.

Methods: SW480 and SW620 cells, in the logarithmic growth phase, were treated with or without the SHP2 inhibitor PHPS1, the activator Trichomide A, EGF, or MMP inhibitors, and randomly assigned to four groups. Additionally, SW480 cells in the logarithmic phase underwent treatments with EGF, the ferroptosis inducer erastin, Trichomide A, or the curcumin analog C1, forming seven groups.

A new potential risk factor for permanent cranial nerve injury following carotid body tumor resection.

Background: To quantify the association between the free distal segment length of the internal carotid artery (FDS-ICA) and permanent cranial nerve injury (p-CNI) following carotid body tumor (CBT) resection.

Methods: This study is a case-control study. We surveyed 109 consecutive patients who underwent CBT resection between June 2015 and June 2020 at our single center.

Resibufogenin suppresses growth and metastasis through inducing caspase-1-dependent pyroptosis via ROS-mediated NF-κB suppression in non-small cell lung cancer.

The purpose of this study is to explore the antitumor properties of resibufogenin (RB) in non-small cell lung cancer (NSCLC) and elucidate its underlying mechanism. A549 and H520 cells were treated with various concentrations of RB with or without NLRP3 inhibitor (MCC950), caspase-1 inhibitor (VX765), or N-acetyl-l-cysteine (an ROS scavenger). Cell counting kit-8 and colony formation assays were conducted to determine cell viability.