Histology and histopathology Vol.39, nº4 (2024)

Ir a Estadísticas

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    Oncogenic miR-106b-5p promotes cisplatin resistance in triple-negative breast cancer by targeting GDF11
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Zhou, Qing; Hu, Qinglin
    Background. Cytoplatin (CDDP) is a standard treatment for triple-negative breast cancer (TNB), but patient resistance to CDDP limits its efficacy. A growing study confirms that microRNAs (miRNAs) are significantly important in breast cancer, especially TNBC. This research was carried out to examine the function of miR-106b-5p in CDDP resistance of TNBC as well as the downstream mechanism. Methods. The miR-106b-5p and growth-differentiation factor 11 (GDF11) expressions in the tissues from TNBC patients and CDDP-treated TNBC cell lines were measured by RT-qPCR. Thereafter, cell proliferation and migration in the presence of CDDP treatment were evaluated via CCK-8 and Transwell assays in the TNBC cells. A xenograft mice model was also established to verify the miR-106b-5p silencing effect on the growth of CDDP resistance TNBC cells in vivo. Luciferase reporter experiments were performed to predict the relationship between miR-106b-5p and GDF11 expression. Results. The results showed that miR-106b-5p was upregulated in the TNBC tumor cells and TNBC cells treated with CDDP and knockdown of this caused inhibition of the TNBC cell lines’ proliferation, migration and suppressed the growth of the TNBC xenografted tumors, in the presence of CDDP treatment. In addition, it was observed that miR-106b-5p can bind to GDF11; as a result in the TNBC tissues and CDDP-treated TNBC cell lines the down-regulation of GDF11 was observed. Moreover, GDF11 silencing promoted CDDP-treated TNBC cell lines’ proliferation and migration and reversed the interference effect of miR-106b-5p. Conclusions. MiR-106b-5p was upregulated in TNBC and this upregulation may promote CDDP resistance of the TNBC cells by targeting GDF11 and inhibiting its expression.
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    Systematic analysis of expression and prognostic significance for MCM family in head and neck squamous cell carcinoma
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Sun, Ercan; Peng, Lu; Liu, Zhe; Yan, Zeng; Chen, Min; Zheng, Jun
    Background. Head and neck squamous cell carcinoma (HNSC) is a common malignant tumor in the world and has a poor prognosis. The family of minichromosome maintenance proteins (MCM) improves the stability of genome replication by inhibiting the rate of DNA replication in eukaryotic cells, thus, small changes in physiological MCM levels would increase the instability of gene replication and increase the incidence of tumor formation, most of which are significantly elevated in multiple cancers. However, the expression of different MCM families in HNSC and their prognostic value remain unclear. Methods. ONCOMINE and GEPIA databases were used to analyze the expression of MCMs in HNSC. The Kaplan-Meier plotter database was used to identify molecules with prognostic values. We collected 77 HNSC tissues and 50 normal tissues to validate the results of the bioinformatics analysis by immunohisto-chemical staining. Results. The expression of MCM3, MCM5 and MCM6 in mRNA and protein levels were higher in HNSC. Moreover, the increased expression of MCM3, MCM5 and MCM6 in mRNA and protein levels predicted better prognosis of HNSC patients. Furthermore, multivariate analysis showed that high expressions of MCM3, MCM5 and MCM6 in protein level may be independent prognostic factors for HNSC patients. Conclusion. The results of this study indicated that MCM3, MCM5 and MCM6 play an important role in occurrence and development in HNSC and might be risk factors for the survival of HNSC patients.
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    miR-638 suppresses cervical cancer progression by inhibiting NCAPG2 under the treatment of Tetrandrine
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Wang, Min; Liu, Kai; Zhou, Zhongming; Geng, Huizhuan
    Background. The interaction of microRNA with Chinese herbal medicines is a promising therapeutic approach for prevention of cervical cancer. Methods. Western blotting or qRT-PCR were carried out to identify the expression of NCAPG2 and miR-638. A tetrandrine (TET) cell model was used to explore the effects of miR-638 and its target gene NCAPG2 using CCK-8, transwell, wound healing, and western blot assays. Furthermore, luciferase activity assay was conducted to measure the interaction among TET, NCAPG2 and miR-638. Results. Under TET treatment, Hela and SiHa cells exhibited repressed cell viability, migration, invasion, and epithelial-mesenchymal transition (EMT), and these effects were further enhanced by high expression of miR-638. In contrast, NCAPG2 expression was low in TET-treated cells and had an opposite effect to that of miR-638. Conclusion. We highlighted that miR-638 suppresses cervical cancer progression by inhibiting NCAPG2 under tetrandrine treatment
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    Cold-shock proteins accumulate in centrosomes and their expression and primary cilium morphology are regulated by hypothermia and shear stress
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Díaz de Cerio, María; Oliván, Sara; Ochoa, Ignacio; García Sanmartín, Josune; Martínez, Alfredo
    Primary cilia act as cellular sensors for multiple extracellular stimuli and regulate many intracellular signaling pathways in response. Here we investigate whether the cold-shock proteins (CSPs), CIRP and RBM3, are present in the primary cilia and the physiological consequences of such a relationship. R28, an immortalized retinal precursor cell line, was stained with antibodies against CIRP, RBM3, and ciliary markers. Both CSPs were found in intimate contact with the basal body of the cilium during all stages of the cell cycle, including migrating with the centrosome during mitosis. In addition, the morphological and physiological manifestations of exposing the cells to hypothermia and shear stress were investigated. Exposure to moderately cold (32°C) temperatures, the hypothermia mimetic small molecule zr17-2, or to shear stress resulted in a significant reduction in the number and length of primary cilia. In addition, shear stress induced expression of CIRP and RBM3 in a complex pattern depending on the specific protein, flow intensity, and type of flow (laminar versus oscillatory). Flow-mediated CSP overexpression was detected by qRT-PCR and confirmed by Western blot, at least for CIRP. Furthermore, analysis of public RNA Seq databases on flow experiments confirmed an increase of CIRP and RBM3 expression following exposure to shear stress in renal cell lines. In conclusion, we found that CSPs are integral components of the centrosome and that they participate in cold and shear stress sensing.
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    microRNA-105-5p protects against chondrocyte injury, extracellular matrix degradation, and osteoarthritis progression by targeting SPARCL1
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Jiang, Dong; Cheng, Shigao; Kang, Pengcheng; Li, Tengfei; Li, Xun; Xiao, Jiongzhe; Ren, Lian
    Objective. Both microRNA (miR)-105-5p and SPARCL1 were discovered to be differentially expressed in osteoarthritis (OA), but their roles and exact mechanisms have not been entirely elaborated. This paper sets out to probe the impact of miR-105-5p/SPARCL1 on chondrocyte injury, extracellular matrix degradation, and osteoarthritis progression. Methods. C28/I2 cells were stimulated with IL-1β to construct an in vitro OA model. C28/I2 cells were transfected with sh-SPARCL1, oe-SPARCL1, or miR-105-5p mimic before IL-1β induction. CCK-8 assay, flow cytometry, and ELISA were adopted to assess cell viability, apoptosis, and inflammatory factor expression, respectively. The binding relationship of miR-105-5p to SPARCL1 was assessed using dual-luciferase reporter assay. After an OA rat model was established, rats underwent intra-articular injection with ago-miR-105-5p. TUNEL was applied to determine cell apoptosis in vivo. mRNA and protein levels were measured by qRT-PCR and western blot, respectively, in vitro and in vivo. Results. IL-1β treatment diminished miR-105-5p expression and augmented SPARCL1 expression in C28/I2 cells. miR-105-5p decreased SPARCL1 expression by targeting SPARCL1. miR-105-5p overexpression or SPARCL1 silencing prominently reversed the decrease in viability and the promotion of inflammatory factor production, cartilage matrix degradation, and apoptosis in IL-1β-stimulated C28/I2 cells. Furthermore, upregulation of SPARCL1 nullified the influence of miR-105-5p overexpression on viability, apoptosis, inflammation, and cartilage matrix degradation in IL-1β-stimulated C28/I2 cells. miR-105-5p overexpression ameliorated knee cartilage tissue injury in OA rats. Conclusion. Conclusively, miR-105-5p exerted suppressive effects on chondrocyte injury, extracellular matrix degradation, and OA progression by targeting SPARCL1.