Nowadays, colorectal cancer is the fourth most common type of tumor all over the world. When diagnosed, ∼50%–60% of tumors have metastasized, thus resulting in a grim prognosis. Chemotherapy is regarded as standard treatment for patients with colorectal cancer, however, limitations of chemotherapy cannot be ignored, such as low selectivity, insufficient concentrations in tumor tissues, and systemic toxicity. Recently, six targeted drugs have been approved by the U.S. Food and Drug Administration (FDA) for treatment of metastatic colorectal cancer (mCRC), including bevacizumab, aflibercept, regorafenib, cetuximab, and panitumumab. The development of these drugs marked significant advancement in the field of mCRC therapy. The addition of biologic agents to chemotherapy has prolonged the median overall survival. Now, many investigational drugs are under clinical trials, of which programmed death (PD)-1/L1 has drawn much attention. In this review, new biologic agents under clinical trials such as MEK/MET/RAS/RAF/PD-1 inhibitors with potentials for mCRC treatment are concluded by describing targeted drugs approved by FDA, to offer new insights into global trends and future development.

Background: The turmeric rhizome yields a medicinal compound called curcumin. Curcumin’s anticancer methods mostly involve blocking cell invasion and proliferation, controlling gene expression, preventing angiogenesis, triggering apoptosis, and inducing ferroptosis. A brand-new nonapoptotic kind of planned cell death is called ferroptosis. Ferroptosis can be initiated through two major pathways: the extrinsic or transporter-dependent pathway, and the intrinsic or enzyme-regulated pathway. It is unknown, therefore, how curcumin and its derivatives prevent cancer by controlling ferroptosis. Purpose: Through this review, we concentrate on the possible anticancer mechanisms of curcumin by means of its effect on ferroptosis; the regulation of iron metabolism, the synthesis of reactive oxygen species, and the targeting of antioxidant pathways represent a few of these processes. Methodology: Retrieve English literature of curcumin and its derivatives in the treatment of tumor by ferroptosis from databases such as Web of Science, etc. Conclusion: This review provides a rationale for the clinical use of curcumin and its derivatives as anticancer agents.

Poly(ADP-ribose) polymerase inhibitors (PARPi) for the treatment of homologous recombination (HR)-deficient cancers have revolutionized cancer treatment in

CD47 is a major innate immune checkpoint molecule that interacts with signal regulatory protein α (SIRPα) to deliver a “don’t eat me&

Background: Colorectal cancer (CRC) is a common and deadly malignancy. Although 5-fluorouracil (5-FU) continues to be a standard therapeutic agent for CRC, the development of resistance substantially compromises its clinical effectiveness. Curcumin, a natural polyphenol, has shown potential in reversing chemoresistance, possibly through ferroptosis-related mechanisms. Purpose: The present work explored the potential of curcumin to restore responsiveness to 5-FU in resistant CRC cells and examined the possible involvement of ferroptosis through a combined bioinformatics and experimental strategy. Materials and Methods: Curcumin-related targets were predicted using SwissTargetPrediction, Super-PRED, and Herbal Ingredients’ Targets (HIT). Protein–protein interaction (PPI) networks, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, as well as ferroptosis-related target screening, were performed using Search Tool for the Retrieval of Interacting Genes/Proteins (STRING), Metascape, and FerrDb. Genes associated with CRC and 5-FU resistance were retrieved from GeneCards and Genomics of Drug Sensitivity in Cancer (GDSC) databases, and intersecting candidates were subsequently mapped using Cytoscape software. In vitro experiments were conducted in HCT8/5-FU cells. Cellular proliferation and viability were evaluated with the Cell Counting Kit-8 (CCK-8) method. Boron-dipyrromethene (BODIPY) 581/591 C11 staining was performed to evaluate lipid peroxidation, whereas intracellular ferrous iron (Fe ²⁺ ) accumulation was determined by flow cytometric analysis. Expression levels of epidermal growth factor receptor (EGFR) and glutathione peroxidase 4 (GPX4) were evaluated by Western blot and reverse transcription quantitative polymerase chain reaction (RT-qPCR). Ferrostatin-1 (Fer-1) was used to investigate the involvement of ferroptosis. Results: Network pharmacology analysis showed that curcumin targets genes and pathways associated with chemoresistance and ferroptosis, with EGFR identified as a key target. In vitro experiments demonstrated that curcumin reduced the proliferative capacity of HCT8/5-FU cells and enhanced the inhibitory effect of 5-FU. Curcumin increased lipid reactive oxygen species (ROS) and intracellular Fe ²⁺ levels, accompanied by reduced mRNA and protein activity of GPX4 and EGFR. Fer-1 partially restored cell viability and reversed the downregulation of ferroptosis-related markers, while intracellular Fe ²⁺ remained elevated. Conclusion: Curcumin restored responsiveness to 5-FU in resistant CRC cells and may be associated with ferroptosis-related mechanisms involving lipid peroxidation, iron metabolism, and EGFR regulation. These findings provide credence to the idea that curcumin could be a useful supplementary tactic for overcoming chemoresistance in CRC.