The radiation resistance of prostate cancer remains the primary obstacle to improve patient survival. This study aimed to investigate the effects of berberine, a commonly used natural product, on the radiosensitivity of prostate cancer. Prostate cancer cell line LNCaP and DU-145 were subjected to hypoxia and/or ionizing radiation (IR), in the presence or absence of berberine treatment. Cell growth and colony formation, and apoptosis were evaluated. Moreover, LNCaP cells were xenografted into nude mice and subjected to IR and/or berberine treatment. The expression of HIF-1α and VEGF in prostate cancer cells and xenografts was detected by Western blot analysis. Berberine increased radiosensitivity of prostate cancer cells and xenografts in a dose dependent manner, and this was correlated with the inhibition of HIF-1α and VEGF expression. Berberine may inhibit the expression of HIF-1α and VEGF and thus confer radiosensitivity on prostatic cancer cells. Berberine has potential application as an adjuvant in radiotherapy of prostatic cancer. The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1519827543125021 .

Objectives: The primary goal of the current study was to investigate the effect of melittin on colorectal cancer (CRC). Methods: The viability of cancer cells was tested using the MTT assay, and the apoptosis of tumour cells was assayed using Annexin V/PI staining in vitro or TUNEL staining in vivo. The in vivo toxicity and efficacy of melittin were assessed in a xenograft mouse model. Results: Melittin inhibited the viability of CRC cell lines and induced apoptosis in SW480 cells by regulating apoptosis-related proteins. Melittin triggered endoplasmic reticulum (ER) stress and caused an imbalance in calcium homeostasis in SW480 cells. An absence of melittin triggered ER stress via the calcium chelating agent BAPTA/AM, and the IP3R inhibitor 2-aminoethoxydiphenyl borate (2-APB) impaired melittin-induced apoptosis in SW480 cells. Melittin treatment suppressed tumour growth but did not affect the body weight of SW480 tumour-bearing mice. Unlike cisplatin and 5-fluorouracil, melittin treatment did not change the biochemical and haematological parameters of the tumour-bearing mice. Finally, in these mice, melittin treatment induced ER stress, which was then blocked by BAPTA/AM, whilst 2-APB impaired the growth inhibitory effect of melittin. Conclusion: Melittin treatment inhibits CRC progression by inducing ER stress and an imbalance in calcium homeostasis.

Background: In the United States, cancer is a leading cause of mortality, with inflammation playing a crucial role in cancer progression and prognosis. Diet, with its capacity to modulate inflammatory responses, represents a potentially modifiable risk factor in cancer outcomes.Methods: This study utilized data from the National Health and Nutrition Examination Survey (NHANES, 1999–2018) to investigate the association between the Dietary Inflammatory Index (DII), which reflects dietary-induced inflammation, and mortality among cancer survivors. A total of 3,011 participants diagnosed with cancer were included, with DII scores derived from dietary recall data. All-cause and cancer-related mortalities served as primary endpoints.Results: The study identified a significant linear positive correlation between higher DII scores and all-cause mortality among cancer survivors. Each unit increase in DII was associated with a 10% higher risk of all-cause mortality (hazard ratio [HR] per 1-unit increase, 1.10; 95% confidence interval [CI], 1.04–1.15). Similarly, a unit increase in DII was associated with a 13% higher risk of cancer-related mortality (HR per 1-unit increase, 1.13; 95% CI, 1.02–1.25). Kaplan–Meier analyses demonstrated higher all-cause mortality rates in individuals with elevated DII scores. Sensitivity analyses confirmed the robustness of these findings.Conclusion: Adoption of an anti-inflammatory diet, characterized by lower DII scores, may improve survival outcomes in cancer survivors. These results emphasize the critical role of dietary interventions in post-cancer care.

Rhabdomyosarcoma (RMS) is a malignant tumor that is more common in children and rarely occurs in adults. Its prognosis mainly depends on the tumor stage and genetic type. In the past few decades, the survival rate of rhabdomyosarcoma has been significantly improved. Embryonal rhabdomyosarcoma (ERMS), alveolar rhabdomyosarcoma (ARMS), and pleomorphic rhabdomyosarcoma (PRMS) are common types of rhabdomyosarcoma. ERMS and ARMS are more common in children, while PRMS is more common in adults and has a poor prognosis. We report a case of a 40-year-old patient with ARMS. His chief complaint was difficulty urinating. The diagnosis was confirmed by puncture biopsy of the prostate, and pelvic lymph node metastasis was already present at the time of diagnosis. The patient underwent seven courses of chemotherapy and proton therapy and five courses of adjuvant chemotherapy. Unfortunately, 8 months after proton beam therapy, the patient showed disease progression (bone metastasis). This case illustrates the difficulties in managing late-stage prostatic alveolar rhabdomyosarcoma and is the first case reported in our hospital to be treated with proton beam therapy in an adult with ARMS of the prostate.

Objective This study aims to investigate the potential of Salvianic acid A (SAA) to enhance the efficacy of anti-PD-1 immunotherapy in triple-negative breast cancer (TNBC), with a focus on elucidating the mechanisms. Methods To explore the effects of SAA on anti-PD-1 therapy efficacy, we established a mouse tumor model using 4T1 breast cancer cells and treated groups with SAA, anti-PD-1 (αPD-1), or their combination. Tumor growth, weight, and survival were monitored. A melanoma mouse model using B16 melanoma cells was also used to validate the efficacy of SAA enhanced immunotherapy. Tumor tissues were analyzed histologically and by flow cytometry to assess immune cell infiltration and function. The expression of immune markers and cytokines was evaluated using immunohistochemistry, Western blot, and quantitative RT-PCR. In vitro experiments were conducted on 4T1, MDA-MB-231, and MDA-MB-453 breast cancer cell lines, as well as CD8 T cells and endothelial cells, to investigate the direct effects of SAA on cell viability, activation, and phenotype maintenance. Additionally, the impact of SAA on high endothelial venules (HEVs) was assessed using immunofluorescence and flow cytometry. Results The combination of SAA and anti-PD-1 therapy significantly inhibited tumor growth and prolonged survival in the 4T1 mouse model and B16 mouse model respectively, compared to controls (P < 0.001). Tumor volumes and weights were consistently lower in the combination group, with no significant weight loss or toxicity observed. Histological analysis revealed increased stromal content and reduced tumor cell density in the SAA + αPD-1 group, indicating enhanced immune cell infiltration and tumor cell death. Flow cytometry showed that SAA significantly increased the infiltration of CD8 T cells and stem-like CD8 T cells (TCF1 and SLAMF6) into the tumor microenvironment when combined with αPD-1 (P < 0.001). The combination also enhanced the expression of IFN-γ and Ki-67 in CD8 T cells, indicating improved functional capacity. Additionally, SAA promoted the formation of HEVs in tumor tissues, as evidenced by increased CD31 and MECA-79 staining (P < 0.001). In vitro, SAA did not directly inhibit breast cancer cell viability or activate CD8 T cells but maintained the high endothelial phenotype in endothelial cells by upregulating key markers such as ACKR1 and CDH5. These findings demonstrate that SAA enhances anti-PD-1 efficacy by modulating the tumor immune microenvironment and promoting HEV formation, without direct cytotoxic effects on cancer cells or immune cells. Conclusion SAA significantly enhances the efficacy of anti-PD-1 therapy by promoting HEV-mediated stem-like CD8 T cells infiltration in TNBC. The combination of SAA and αPD-1 represents a promising therapeutic strategy that warrants further exploration in preclinical and clinical settings.

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