Histology and histopathology Vol.40, nº9 (2025)
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- PublicationOpen AccessTRIB1 facilitates the proliferation and migration of ovarian cancer cells by inducing EMT progression(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Shi Guangyan; Holgersson Kristian; Xin Zhen; Szekely Laszlo; Du Qiqiao; Jing Xu; Biología Celular e HistologíaAim. Ovarian cancer (OC) is a fatal female malignant tumor that severely impacts the health of women worldwide. Due to the lack of diagnostic biomarkers, 70% of OC patients are considered in the advanced stage at the first diagnosis. Exploring novel biomarkers for OC diagnosis has become an urgent clinical need to address. TRIB1 is a newly discovered oncogene in several malignant tumors, including acute myeloid leukemia, prostate cancer, and breast cancer. However, the biological function of TRIB1 in OC remains uncertain and, therefore, was explored in the present study. Methods. Levels of TRIB1 in OC and normal tissues were evaluated in the GEPIA database. TRIB1-KD was constructed in ES-2 cells and TRIB1-OE was constructed in OVCAR3 cells using a siRNA and OE vector, respectively. The proliferation ability was determined using the CCK-8 and clone formation assays. The migration ability was detected using the wound healing and Transwell assays. The expression of epithelial-mesenchymal transition (EMT) biomarkers was determined using western blotting. Results. TRIB1 was markedly upregulated in OC tissues compared with normal ovarian tissues in the GEPIA database. The TRIB1 level was slightly altered among ES-2, CAOV3, and SKOV3 cells, with the highest expression in ES-2 cells, which was greatly reduced in OVCAR3 cells. In TRIB1-KD ES-2 cells, a remarkably reduced proliferation ability was observed with the CCK-8 and clone formation assays, accompanied by a reduction in migration distance in the Wound healing assay and the number of migrated cells in the Transwell assay. In contrast, in TRIB1-OE OVCAR3 cells, increased proliferation ability was observed, accompanied by increased migration distance and number of migrated cells. Furthermore, EMT progression was markedly repressed in TRIB1-KD ES-2 cells and remarkably enhanced in TRIB1-OE OVCAR3 cells. Conclusion. TRIB1 facilitated the proliferation and migration of OC cells by enhancing EMT progression
- PublicationOpen AccessClinical significance of ALDH1A1 and Ki67 expression in women with breast carcinoma(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Zong Yuxuan; Ma Shuang; Yin Jiaxin; Qiao Na; Zhang Dongmei; Niu Zhaoyang; Zhao Ye; Zhou Fei; Biología Celular e HistologíaBackground. Breast cancer is the most prominent cancer among women worldwide, with a two-fold incidence in China compared to the worldwide incidence. ALDH1A1, catalyzing the oxidation of intracellular aldehydes and converting retinol into retinoic acid, serves as a biomarker of early stem cell differentiation. Ki67 levels are prognostic or residual risk biomarkers after primary therapy and can predict the effects of systemic therapies or monitor patients for sustained response or resistance to the administered therapies. This study aimed to investigate the correlation between ALDH1A1 and Ki67 expression and clinicopathological parameters among women with breast cancer. Methods. Breast cancer tissue specimens were obtained from the Department of Pathology at the First Hospital of Qiqihar. Indirect fluorescent immunostaining was used to assess the expression of ALDH1A1 and Ki67 in breast cancer and healthy tissues. Associations between ALDH1A1 and Ki67 expression and clinicopathological parameters of breast cancer were evaluated using the chi-square test. A p-value less than 0.05 was considered statistically significant. The correlation between ALDH1A1 and Ki67 expression was assessed using Spearman’s rank correlation analysis. Results. ALDH1A1 and Ki67 were upregulated in breast cancer tissue compared with normal breast tissue (p<0.05). Furthermore, ALDH1A1 expression was further upregulated with an advancement in breast cancer grade, i.e., ALDH1A1 expression levels were higher in patients with stage III/IV breast cancer than in those with stage I/II breast cancer. Furthermore, ALDH1A1 and Ki67 were upregulated in the presence of lymphatic metastasis. Conclusion. ALDH1A1 may be considered a pathognomonic marker for breast cancer. ALDH1A1 and Ki67 expression are significantly positively correlated in women with breast cancer.
- PublicationOpen AccessMLH1 and MSH2 expression in endometrial cancer - microscopic and computer assessment of immunohistochemical method(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Rogaliński Jan; Przewoźny Stanisław; De Mezer Mateusz; Markowska Anna; Markowska Janina; Żurawski Jakub; Biología Celular e HistologíaObjective. We aimed to compare MLH1 and MSH2 protein expression and Mismatch repair (MMR) status with clinical data: diagnosis, grading, and staging. Moreover, we wanted to assess any correlation between two immunohistochemical assessments: classic microscopic and computer analysis performed by a calibrated program. Materials and methods. Our studies were conducted on 95 cases of endometrial cancer. For each, we performed H+E staining and immunohistochemistry (IHC) of two MMR status proteins: MLH1 and MSH2. Two independent researchers assessed IHC on a 0 to ++++ scale. We classified cases as MMR-deficient based on the microscopic assessment of the absence of expression of at least one protein. For computer analysis, we used Olympus cellSens software to measure the positive IHC reaction area in μm2 in five fields of vision. Results. Despite using two different assessment methods, we did not identify any statistically significant relationship between diagnosis, grading, staging, MMR protein expression, and MMR status. However, we found a strong correlation between computer analysis and semi-quantitative microscopic assessment (r=0.59 for MLH1 and r=0.76 for MSH2; p<0.001 for both). Furthermore, we revealed that computer measurement of the expression area could be a good objective prediction test for microscopic analysis (p<0.001). Conclusion. We did not find a relationship between MMR status and grading, staging, or diagnosis. However, we present a novel approach to immunohisto-chemical assessment using computer analysis. It allows us to carry out more objective and accurate studies with the IHC method
- PublicationOpen AccessGentiopicroside alleviates neuroinflammation in Parkinson's disease by mediating microglial pyroptosis via the NF-κB/NLRP3/GSDMD pathway(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Shen Hong; Song Hui; Sun Qiang; Biología Celular e HistologíaObjective. The study aimed to evaluate the therapeutic potential of gentiopicroside (GPS) in Parkinson's disease (PD) through both in vitro and in vivo experiments, focusing on elucidating the underlying mechanisms of its action. Methods. To achieve this, a PD model was established in C57BL6 mice using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), followed by assessment of behavioral changes, pathological alterations, microglial activation, and neuro-inflammation. Simultaneously, a cellular PD model was developed in the BV-2 mouse microglia cell line by exposing them to 1-methyl-4-phenyl-pyridinium (MPP+). The expression of pro-inflammatory molecules was quantified using enzyme-linked immunosorbent assay (ELISA), while pyroptosis was analyzed by flow cytometry with caspase-1/PI double staining. The expression of key factors in the nuclear factor-kappa B (NF-κB)/NOD-like receptor thermal protein domain-associated protein 3 (NLRP3)/gasdermin D (GSDMD) signaling pathway was determined by immunoblotting. Results. The findings revealed that GPS effectively mitigated motor deficits, neurological impairments, microglial activation, and neuroinflammation in the MPTP-induced mouse model of PD. Additionally, GPS protected BV-2 cells from MPP+-induced inflammatory cytokine production and pyroptosis. Mechanistic studies indicated that GPS may exert its neuroprotective effects by inactivating the NF-κB/NLRP3/GSDMD-mediated pyroptotic pathway in both in vivo and in vitro settings. Conclusion. GPS exhibits neuroprotective effects in PD by suppressing microglia-mediated neuro-inflammation and pyroptosis, suggesting its potential as a favorable therapeutic agent for PD treatment
- PublicationOpen AccessThe synergetic effect of edaravone and scutellarin in the MPP(+)-induced cell model of Parkinson's disease(Universidad de Murcia, Departamento Histología e Histopatología, 2025) Wei Wei; Wu Jing; Zhang Dandan; Xu Shoucheng; Wang Yi; Li Xuezhong; Yu Ming; Chen Xiaopeng; Biología Celular e HistologíaParkinson's disease (PD) is a limb movement disorder caused by the degeneration of brain neurons and seriously affects the quality of life of the elderly. However, the current drugs are symptomatic treatments that cannot prevent or delay the development of the disease. Targeted therapy for pathogenesis may be the direction of development in the future. Oxidative stress and the inflammatory response are involved in the pathogenesis of PD. Edaravone and scutellarin have been studied in antioxidant and anti-inflammatory reactions. The focus of this study is whether there is synergy between the two and its mechanism. Through research, we found that edaravone and scutellarin at different dose combinations have synergistic effects in 1-methyl-4-phenylpyridinium (MPP+)-induced PC12 cells using the Chou-Talalay joint index method. According to the CompuSyn software calculation, the results showed that the combination index (CI) of the combined application of 15 μM edaravone and 15 μM scutellarin was the lowest, indicating that the synergistic effect was the best. Compared with the single drug, the synergy increased superoxide dismutase (SOD) and reduced glutathione (GSH) levels, reduced the levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and enhanced the anti-apoptosis ability in the MPP(+) induced cell model of PD.
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