modified-entry-hole-closure-method-for-esophagojejunostomy-totally

Modified Entry Hole Closure Method for Esophagojejunostomy in Totally Laparoscopic Total Gastrectomy: A Safe, Repeatable Method Using a Barbed Suture

Totally laparoscopic total gastrectomy (TLTG) has not been widely used to date because of the risk of postoperative complications and difficulty in ...

The First Affiliated Hospital of Soochow University

Tumor hypoxia has been recognized as a characteristic of the tumor microenvironment and promotes metastasis in a variety of types of cancer. However, in lung cancer, the role of hypoxia-inducible factor 1α (HIF-1α) in modulating the cellular response to the inflammation-related microenvironment remains unclear. In the present study, enhanced expression of HIF-1α accompanied by an increased ROS level was observed in lipopolysaccharide (LPS)-stimulated non-small cell lung cancer (NSCLC) cells. In addition, propofol, a general anesthetic, was found to significantly reduce the LPS-induced upregulation of HIF-1α and ROS in a dose-dependent manner. Further study showed that propofol may antagonize the role of LPS in activating HIF-1α through attenuating the protein stability and nuclear localization of HIF-1α. Moreover, knockdown of HIF-1α attenuated expression of mesenchymal marker, vimentin, but promoted the expression of epidermal marker, E-cadherin, in the LPS-treated NSCLC cells. Notably, LPS-induced epithelial-to-mesenchymal transition (EMT) was notably suppressed by propofol treatment. Consistently, a wound healing assay revealed that propofol abrogated LPS-stimulated migration of NSCLC cells while overexpression of HIF-1α reversed the effects of propofol. Similarly, we investigated the influence of propofol on the invasive capability of NSCLC cells. Western blot and RT-PCR analyses indicated that both knockdown of HIF-1α and treatment of propofol attenuated the LPS-activated expression of MMP2 and MMP9 which are necessary for tumor invasion. However, results from the Transwell assay confirmed that propofol also suppressed cell invasion by decreasing HIF-1α expression in the LPS-treated NSCLC cells. Analysis of clinical specimens demonstrated abnormal expression of HIF-1α in NSCLC tissues and a poor prognosis in patients with elevated HIF-1α expression. Thus, the present study suggests a potential strategy for NSCLC by targeting HIF-1α.

Propofol suppresses LPS-induced nuclear accumulation of HIF-1α and tumor aggressiveness in non-small cell lung cancer.

 Colorectal cancer (CRC) is the primary cause of cancer-related mortality globally. Research indicates that CRC is associated with the dysregulation of NLRP3 expression. Therefore, further investigation is warranted into the correlation between NLRP3 and CRC proliferation and metastasis.  NLRP3 and GLI1 expression levels were assessed in tumor tissues using qPCR and bioinformatics analysis. We performed Western blot, CCK8 assay, Colony formation assay, Transwell assay, and mouse xenografts to investigate the effects of NLRP3 on the proliferation and migration of CRC cells while identifying the potential underlying mechanisms involved.  Our research demonstrated that elevated NLRP3 levels in CRC tissue correlated with adverse patient outcomes. Enhanced NLRP3 expression significantly affects progression-free and relapse-free survival. Furthermore, suppressing NLRP3 expression effectively inhibited the proliferation and migration of CRC cells while impeding epithelial-mesenchymal transition (EMT) signaling and the S6K1-GLI1 pathway. Notably, the mouse xenotransplantation study validated that deleting NLRP3 suppresses CRC development.  NLRP3 facilitates CRC progression via the EMT and the S6K1-GLI1 signaling pathway, providing a promising target against CRC patients.

Article	Year
Propofol suppresses LPS-induced nuclear accumulation of HIF-1α and tumor aggressiveness in non-small cell lung cancer. Oncology reports\| PubMed ID: 28426124	2017
NLRP3 promotes the proliferation and metastasis of colorectal cancer by regulating the S6K1-GLI1 signaling pathway. Journal of Cancer\| PubMed ID: 39744485	2025

Pei Yang

Biography

JoVE Journal Publications

Other Publications