The aim of the present study was to investigate whether fraction from Lycium barbarum polysaccharide (LBP) could reduce immunotoxicity and enhance antitumor activity of doxorubicin (Dox) in mice. A water-soluble LBP fraction, designated LBP3, was isolated from edible Chinese herbal Lycium barbarum and used in this study. To investigate the effect of LBP3 on Dox-induced immunotoxicity, tumor-free mice were used and treated with either normal saline, Dox, or Dox plus LBP3. To investigate the effect of LBP3 on antitumor activity of Dox, H22 tumor-bearing mice were used and treated with either normal saline, Dox, LBP3, or Dox plus LBP3. The results showed that LBP3 did not protect against the body weight loss caused by Dox, but it promoted the recovery of body weight starting at day 5 after Dox treatment in tumor-free mice. LBP3 also improved peripheral blood lymphocyte counts, promoted cell cycle recovery in bone marrow cells, and restored the cytotoxicity of natural killer cells. Furthermore, in H22 tumor-bearing mice, LBP3 enhanced antitumor activity of Dox and improved peripheral blood lymphocyte counts and the cytotoxicity of splenocytes. In brief, our results demonstrated that LBP3 could reduce the immunotoxicity and enhance antitumor activity of Dox.
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http://dx.doi.org/10.1177/1534735417753544 | DOI Listing |
Cell Biol Toxicol
January 2025
Division of Abdominal Tumor Multimodality Treatment, Cancer Center and Laboratory of Molecular Targeted Therapy in Oncology, West China Hospital, Sichuan University, 610041, Chengdu, Sichuan Province, China.
Sorafenib (Sora) is a first-line treatment for patients with advanced hepatocellular carcinoma (HCC). It can significantly improve the survival rate of patients with advanced HCC, but it is prone to drug resistance during treatment, so the therapeutic effect is extremely limited. Here, we demonstrate that an elevated expression of protein kinase p38γ in hepatocellular carcinoma cells diminishes the tumor cells' sensitivity to Sora.
View Article and Find Full Text PDFActa Biomater
January 2025
College of Basic Medical Sciences, Chongqing Medical University, Chongqing 400016, China. Electronic address:
Cuproptosis is a newly discovered mode of cell death, which is caused by excess copper and results in cell death via the mitochondrial pathway. However, the complex tumor microenvironment (TME) is characterized by many factors, including high levels of glutathione and lack O, limit the application of traditional cuproptosis agents in antitumor therapy. Herein, we report a hyaluronic acid modified copper-manganese composite nanomedicine (CMCNs@HA) to remodel the TME and facilitate efficient cuproptosis in tumor.
View Article and Find Full Text PDFNat Commun
January 2025
Institute for Advanced Biosciences, Team: Epigenetics, Immunity, Metabolism, Cell Signaling & Cancer, Inserm U 1209, CNRS UMR 5309, Univ. Grenoble Alpes, Grenoble, France.
Dendritic cells (DC) are key players in antitumor immune responses. Tumors exploit their plasticity to escape immune control; their aberrant surface carbohydrate patterns (e.g.
View Article and Find Full Text PDFCell Death Discov
January 2025
School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032, China.
Methyltransferase-like 1 (METTL1)-mediated m7G modification is a common occurrence in various RNA species, including mRNAs, tRNAs, rRNAs, and miRNAs. Recent evidence suggests that this modification is linked to the development of several cancers, making it a promising target for cancer therapy. However, the specific role of m7G modification in cutaneous squamous cell carcinoma (cSCC) is not well understood.
View Article and Find Full Text PDFJ Adv Res
January 2025
Cancer Institute, Xuzhou Medical University, 209 Tongshan Road, Xuzhou 221004 Jiangsu, China; Center of Clinical Oncology, The Afliated Hospital of Xuzhou Medical University, 99 West Huaihai Road, Xuzhou 221002 Jiangsu, China; Jiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Xuzhou Medical University, 209 Tongshan Road, Xuzhou 221004 Jiangsu, China. Electronic address:
Introduction: Hypericin (HP), a natural photosensitizer, has demonstrated great efficacy in photodynamic therapy (PDT) for cancer treatment. In addition to the induction of apoptosis and necrosis through reactive oxygen species (ROS) generation, the therapeutic mechanisms and targets of PDT-HP remain unknown.
Objectives: To investigate the direct targets and mechanisms of action of photoactivated hypericin in the inhibition of triple-negative breast cancer (TNBC).
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