Gastrointestinal (GI) malignancies, including esophageal cancer, gastric cancer, and colon cancer, are associated with high mortality rates worldwide. Thymoquinone is one of the main bioactive components of Nigella sativa, and it has been documented to have anticancer effects including GI cancer. Thymoquinone inhibits GI cancer progression by inducing cell cycle arrest, apoptosis, and oxidative stress and inhibiting inflammation, migration, invasion, metastasis, histone deacetylases, STAT3, PI3K/AKT/mTOR, and Wnt/β-catenin signaling pathways. Although the beneficial effects of thymoquinone have been documented, some limitations, including poor bioavailability and hydrophobicity, have hindered its clinical application. Nanotechnology approaches bypass these limitations. In this review article, we outline the different cellular and molecular pathways influenced by thymoquinone and its nanoformulations in GI cancer.
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http://dx.doi.org/10.1007/s00210-025-03861-1 | DOI Listing |
Cancer Discov
March 2025
University of California, San Francisco, San Francisco, CA, United States.
Historical studies performed nearly a century ago using mouse skin models identified two key steps in cancer evolution: initiation, a likely mutational event, and promotion, driven by inflammation and cell proliferation. Initiation was proposed to be permanent, with promotion as the critical rate-limiting step for cancer development. Here, we carried out whole genome sequencing to demonstrate that initiated cells with thousands of mutagen-induced mutations can persist for long periods and are not removed by cell competition or by immune intervention, thus mimicking the persistence of cells with cancer driver mutations in normal human tissues.
View Article and Find Full Text PDFChemMedChem
March 2025
Donghua University, Pharmaceutical Science & Technology, CHINA.
A novel pheophorbide derivative, trimethyl-152-[L-aspartyl]pheophorbide a was synthesised and investigated for anti-tumor activity. The prepared photosensitizer had good absorption in the phototherapeutic window and high ROS yields. It exhibited excellent phototoxicity higher than reference compound m-THPC when irradiated by 650 nm light in vitro, and obvious photodynamic anti-tumor effect in vivo.
View Article and Find Full Text PDFIt is known that inhibition of the endoplasmic reticulum transmembrane signaling protein (ERN1) suppresses the glioblastoma cells proliferation. The present study aims to investigate the impact of inhibition of ERN1 endoribonuclease and protein kinase activities on the , , and gene expression in U87MG glioblastoma cells with an intent to reveal the role of ERN1 signaling in the regulation of expression of these genes. The U87MG glioblastoma cells with inhibited ERN1 endoribonuclease (dnrERN1) or both enzymatic activities of ERN1 (endoribonuclease and protein kinase; dnERN1) were used.
View Article and Find Full Text PDFEndocr Regul
January 2025
1Endocrinology and Internal Medicine Department, Fattouma Bourguiba University Hospital, Monastir, Tunisia.
Pituitary neuroendocrine tumors (PitNETS) are common intracranial tumors, but extrasellar or ectopic PitNETS are very rare and supposed to originate from some pituitary remnants. They are mostly found in sphenoidal sinus. But particularly, ectopic clival PitNETS are highly aggressive and can cause bone invasion and can be misdiagnosed as other lesions of the skull base such as chordomas.
View Article and Find Full Text PDFEndocr Regul
January 2025
1Department of Molecular Biology, Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv, Ukraine.
For the effective growth of malignant tumors, including glioblastoma, the necessary factors involve endoplasmic reticulum (ER) stress, hypoxia, and the availability of nutrients, particularly glucose. The ER degradation enhancing alpha-mannosidase like protein 1 (EDEM1) is involved in ER-associated degradation (ERAD) targeting misfolded glycoproteins for degradation in an N-glycan-independent manner. EDEM1 was also identified as a new modulator of insulin synthesis and secretion.
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