Rapeseed protein, an abundant by-product of the vegetable oil industry, is rich in essential amino acids and represents a promising source of antitumor peptides. However, the purification, characterization and mechanistic studies of antitumor peptides derived from rapeseed protein remain limited. Rapeseed protein was hydrolyzed using four proteases (alkaline protease, compound proteinase, flavourzyme and trypsin), followed by ultrafiltration and purification using gel filtration and semi-preparative HPLC. Purified peptides were identified by liquid chromatography-tandem mass spectrometry (LC-MS/MS) and antitumor activities were evaluated against HepG2, MKN-28, A549 and MCF-7 cells using the 3-(4,5-dimethyl thiazole-2-yl)-2,5-diphenyl tetrazolium bromide (i.e. MTT) assay. At 1 mg mL-1, the < 1 kDa fraction showed the strongest inhibitory effects, with inhibition rates of 55.22% ± 0.45%, 60.54% ± 0.84%, 65.33% ± 0.84% and 62.78% ± 1.57%, respectively. Five novel peptides (DHHAPQL, GVIRPPL, NDGNQPL, THPGVAQ and VTDGEAH) were identified. Among them, GVIRPPL exhibited the highest activity, with IC₅₀ values ranging from 1.14 to 1.69 mm. Mechanistic analysis showed that the reactive oxygen species (ROS) level of HepG2 cells treated with 2.0 mm rapeseed antitumor peptide GVIRPPL increased by 50.6% and reduced mitochondrial membrane potential by 53.7%, indicating that rapeseed antitumor peptides can exert antitumor effects by inducing ROS production and interfering with mitochondrial membrane potential, at the same time as having no obvious cytotoxicity to normal human hepatocytes. This study systematically isolated and identified novel antitumor peptides from rapeseed protein hydrolysates and further explored their antitumor activity and mechanisms of action, providing a scientific basis for the high-value utilization of rapeseed protein and the development of antitumor bioactive components for functional food applications. © 2026 Society of Chemical Industry.

Synthesis and evaluation of methoxyquinazoline sulfonamide derivatives as bifunctional molecular targeting tumor related inflammation and anti-EGFR triple-mutation.

Nebivolol-induced bi-directional modulation of intracellular kinases contributes to the inhibition of triple-negative breast cancer.

The plant Cinnamomum tamala (Buch.-Ham.) T. Nees & C.H. Ebern. (Family: Lauraceae) is commonly known as 'tejpaat' in India, has leaves and bark reported to possess anticancer, immunomodulatory, antidiabetic, and diuretic activities. The objective of the present study was to explore the antitumor potential of the chloroform extract of Cinnamomum tamala leaves (CTCE) in BALB/c mice against Ehrlich's Carcinoma (EC). Based on preliminary in-vitro cytotoxicity studies, CTCE was selected for an in-vivo antitumor study. Anticancer activity of CTCE was evaluated in BALB/c mice against EC at the doses of 50, 100, 250, and 500 mg/kg body weight. CTCE was administered for 15 consecutive days after induction of the tumor. After 24 hours from the last administered dose and 18 hours of fasting, half of the mice were sacrificed, while the other half was kept alive to evaluate any potential for increasing the lifespan. The antitumor effect of CTCE was assessed by evaluating tumor volume, hematological parameters, and the life span of the EC-bearing host. CTCE showed a significant decrease (p<0.05) in tumor volume and increased the lifespan of EC tumor-bearing mice in a dose-dependent manner compared with the untreated group. The hematological profile, including RBC count, hemoglobin, WBC count, and DLC, was also improved upon treatment. C. tamala chloroform extract (CTCE) showed significant anticancer potential by reducing cell viability, inhibiting tumor growth, and prolonging survival without toxicity, suggesting it as a promising source of bioactive compounds for anticancer drug development. The results suggest that CTCE exhibits dose-dependent anticancer activity in comparison with EC control mice and demonstrates significant effects relative to doxorubicin. Its antitumor activity may be attributed to the presence of active constituents within the extract. This investigation also highlights recent advancements in intellectual property rights and patent strategies related to plant-derived anticancer agents.

Levistolide A induces endoplasmic reticulum stress-triggered apoptosis via ATF6 in triple-negative breast cancer.

Betulinic acid induces lysosome-dependent death in prostate cancer by targeting DDX5.

Pituitary tumors, as common intracranial neoplasms, present challenges in clinical management because of high postoperative recurrence rate, drug resistance and pronounced side effects. Astragaloside IV (AS‑IV), the primary active component of the traditional Chinese herb Astragalus membranaceus, has antitumor activity in numerous types of cancer. However, its effects and mechanisms in pituitary tumors remain unclear. The present study aimed to investigate the effects of AS‑IV on proliferation and apoptosis of pituitary tumor cells and to elucidate its molecular mechanisms. Cell Counting Kit‑8 (CCK‑8), TUNEL, EdU, immunohistochemistry (IHC), and Western blotting, among others, showed that AS‑IV significantly suppressed the viability of the rat pituitary tumor cell lines GH3 and MMQ in a concentration‑ and time‑dependent manner while inducing apoptosis. Tubulin β4B Class IVb (TUBB4B) was highly expressed in pituitary tumor tissue and its overexpression promoted cell proliferation while inhibiting apoptosis. AS‑IV bound TUBB4B with high affinity, forming a stable complex. TUBB4B regulation influenced pituitary tumor cell sensitivity to AS‑IV, with AS‑IV demonstrating enhanced antitumor efficacy in TUBB4B‑overexpressing tumors. TUBB4B activated the ERK/MAPK signaling pathway by upregulating Stathmin 1 (STMN1) expression, which promoted G1/S phase transition. The ERK‑specific inhibitor U0126 reversed this pro-proliferative effect. To the best of our knowledge, the present study is the first to reveal that AS‑IV inhibits pituitary tumor proliferation and promotes apoptosis by targeting TUBB4B to regulate the STMN1‑ERK signaling axis, providing a novel theoretical basis and potential strategies for traditional Chinese medicine treatment and molecular targeted research on pituitary tumors.

Structural characterization and antitumor activity via immune modulation of an α-glucan from Grifola frondosa.

Design, synthesis and anti-tumor activation of β-carboline alkaloids derivatives from Picrasma quassioides.

This multicentre, modular, Phase 1 study evaluated escalating doses of ATR (ataxia telangiectasia and Rad3-related kinase) inhibitor ceralasertib plus PD-L1 inhibitor durvalumab in patients with previously treated advanced/metastatic non-small-cell lung cancer (NSCLC) or head and neck squamous cell carcinoma (HNSCC). Patients received ceralasertib 80/160/240 mg twice-daily (BID) or 320 mg once-daily (QD) for 7 (Days 22-28) or 14 (Days 15-28) days, plus durvalumab 1500 mg (Day 1), per 28-day cycle. The primary objective was to investigate the safety/tolerability of the combination. Sixty patients were treated. Two patients had dose-limiting toxicities of: Grade 3 thrombocytopenia with Grade 3 anaemia (ceralasertib 320 mg QD for 14 days); and Grade 4 thrombocytopenia with Grade 3 neutropenia accompanied by systemic chest infection (ceralasertib 240 mg BID for 14 days). Overall, 59 (98.3%) patients had treatment-emergent adverse events; 31 (51.7%) had grade ≥3 events. The recommended Phase 2 dose was durvalumab 1500 mg (Day 1) plus ceralasertib 240 mg BID (Days 15-28). Five (8.3%) patients had objective responses; 31 (51.7%) had stable disease. Pharmacodynamic activity (pRAD50 increase) was observed in 10/14 paired biopsies. Ceralasertib plus durvalumab was tolerated and associated with antitumour activity in advanced/metastatic NSCLC and HNSCC. NCT02264678.

Targeted delivery of doxorubicin via cholesteryl-modified cyclodextrin: Antitumor activity in breast, ovarian, and cervical cancer cell lines.

Usenamine a potentiates anti-CRC activity of sorafenib by inducing autophagy and inhibiting YAP pathway through targeting SOD2.

Deziyangxin (DZYX) is a classical Tibetan multi-herb prescription recorded in Jing Zhu Ben Cao and traditionally used for conditions characterized by blood stasis, phlegm-heat accumulation, and tumor-like masses. Despite its long-standing clinical use, the pharmacological basis underlying its potential anti-tumor activity remains insufficiently understood. This study aimed to evaluate the anti-tumor efficacy of DZYX in non-small cell lung cancer (NSCLC) and to explore its potential mechanisms with emphasis on tumor immune microenvironment modulation. Serum pharmacochemistry was performed using LC-MS/MS to identify circulating constituents of DZYX. A syngeneic Lewis lung carcinoma (LLC) mouse model was established in mice, which were treated with DZYX by oral gavage at 78.5mg/kg or 157mg/kg for 25 days. Tumor growth and histopathology were evaluated, while transcriptomic analysis, network pharmacology, flow cytometry, and immunohistochemistry were used to investigate molecular pathways and immune cell infiltration. LC-MS/MS identified 167 circulating components derived from DZYX. DZYX treatment significantly suppressed tumor growth and induced tumor necrosis in LLC-bearing mice. Transcriptomic and enrichment analyses indicated modulation of chemokine signaling, T-cell activation, and innate immune pathways. Flow cytometry and immunohistochemistry further demonstrated increased infiltration of CD4+ and CD8+ T cells, NK cells, and B cells within tumor tissues and spleens. Enhanced intratumoral Granzyme B and IFN-γ signals suggested increased cytotoxic immune activity. DZYX exerts anti-tumor activity in NSCLC associated with remodeling of the tumor immune microenvironment and multi-pathway molecular regulation. These findings provide mechanistic support for the traditional use of DZYX in tumor-related disorders and highlight its potential as an immunomodulatory candidate for lung cancer therapy.

Iodinated contrast agents decrease the activity of multidrug resistance protein, cell migration, and induce cell death in different tumor cell lines and glioblastoma spheroids.

A flaxseed oil body-based delivery system integrating calcium overload and lipid peroxidation for immunogenic cell death-driven immunotherapy.

Design, synthesis, and in vitro/in vivo biological evaluation of Artesunate-Ebselen derivatives: GPX4-targeted ferroptosis induction and synergistic antitumor immune activation in colorectal cancer.

Cancer therapy is increasingly shaped by delivery platforms designed to overcome the limitations of conventional chemotherapy and radiotherapy. Among these, bacterial outer membrane vesicles (OMVs) have emerged as versatile nanocarriers with intrinsic tumor-interacting properties, immunomodulatory capacity, and amenability to bioengineering. Their lipid bilayer composition not only enhances stability and cellular uptake but also intersects with tumor lipid metabolism-an axis increasingly recognized as central to oncogenesis, immune evasion, and therapeutic resistance. Here, we review mechanistic links between OMV lipid composition and autophagy regulation and discuss how engineered OMVs can be used to modulate tumor metabolism, immune responses, and therapy sensitivity. By influencing lipid-autophagy crosstalk, OMVs function as more than passive delivery vehicles; they can actively engage intracellular stress pathways and metabolic dependencies. Autophagy, a context-dependent regulator of cancer survival and suppression, is particularly relevant, as OMVs can deliver bioactive lipids, proteins, or nucleic acids that either promote immunogenic stress responses or attenuate tumor-protective autophagy. Preclinical examples-including doxorubicin-loaded OMVs and PD-1-engineered OMVs-illustrate how these principles translate into enhanced anti-tumor efficacy and immune activation. We further discuss how integration with lipidomics, systems biology, and artificial intelligence-guided design may improve OMV engineering and therapeutic predictability. Collectively, these advances position OMVs as a promising, though still emerging, platform for precision oncology.

Modular metabolic engineering of Yarrowia lipolytica and semi-rational design of CYP716A520 for enhanced betulinic acid biosynthesis.

Aconitum septentrionale Koelle extract alleviates cigarette smoke and lipopolysaccharide-induced chronic obstructive pulmonary disease in mice by modulating the MAPK pathway.

A macroporous frit capillary electrophoresis method for discovery of tumor-targeted components from complex natural medicine mixtures.