Instituto Multidisciplinario de Investigaciones Biológicas San Luis (IMIBIO-SL) CONICET, San Luis, Argentina; Universidad Nacional de San Luis, San Luis, Argentina.
Published: October 2016
AI Article Synopsis
Article Abstract
In the last 15 years, increasing evidences demonstrate a strong link between sphingosine-1-phosphate (S1P) and both normal physiology and progression of different diseases, including cancer and inflammation. Indeed, numerous studies show that tissue levels of this sphingolipid metabolite are augmented in many cancers, affecting survival, proliferation, angiogenesis, and metastatic spread. Recent insights into the possible role of S1P as a therapeutic target has attracted enormous attention and opened new opportunities in this evolving field. In this review, we will focus on the role of S1P in cancer, with particular emphasis in new developments that highlight the many functions of this sphingolipid in the tumor microenvironment. We will discuss how S1P modulates phenotypic plasticity of macrophages and mast cells, tumor-induced immune evasion, differentiation and survival of immune cells in the tumor milieu, interaction between cancer and stromal cells, and hypoxic response.
Background: Since the emergence of the hot topic of "ferroptosis," numerous studies have explored its role in hepatocellular carcinoma (HCC), revealing its significance in the disease's pathogenesis, progression, and treatment. However, there remains a significant gap in the quantitative analysis of ferroptosis in HCC. Therefore, this study aims to comprehensively assess the research progress and evolution in this field through bibliometric and citation analysis.
Pancreatic ductal adenocarcinoma (PDAC) is characterized by its poor prognosis. Traditional Japanese herbal medicine (Kampo), such as Juzentaihoto (a standardized combination of 10 herbal extracts), has shown immune modulatory effects, modulation of microcirculation, and amelioration of fatigue. It is administered to patients to prevent deterioration of cachexia and counteract side effects of chemotherapy.
Neural invasion is one of the most common routes of invasion in pancreatic cancer and it is responsible for the high rate of tumor recurrence after surgery and the pain generation associated with pancreatic cancer. Several molecules implicated in neural invasion are also responsible for pain onset including NGF belonging to the family of neutrophins. NGF released by cancer cells can sensitize sensory nerves which in turn results in severe pain.
Small-cell lung cancer (SCLC) is a refractory cancer with rapid growth and high aggressiveness. Extensive-stage SCLC is initially sensitive to chemotherapy; however, drug resistance and recurrence occur rapidly, resulting in a poor survival outcome due to lack of subsequently efficient therapy. The emergence of immune checkpoint inhibitors (ICIs) generated a new landscape of SCLC treatment and significantly prolonged the survival of patients.
Background: Migrasomes are newly identified organelles on the retracting fibers of migrating cells, involved in releasing signaling molecules, expelling damaged mitochondria, and facilitating intercellular communication through phagocytosis. TSPAN4, a key regulator of migrasome formation, is a valuable marker for visualizing these organelles. However, its role in cancer remains unclear.
