Histology and histopathology Vol.39, nº4 (2024)

Ir a Estadísticas

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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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    Targeting eIF5A2 reduces invasion and reverses chemoresistance in SCC-9 cells in vitro
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Gao, Jinbo; Li, Peng
    Background and Aims. Eukaryotic translation initiation factor 5A2 (EIF5A2) has been reported to be involved in metastasis and chemotherapy resistance in many human cancers. However, the effect and mechanism of EIF5A2 in oral cancer cells are unknown. Here, we investigated the effects of targeting EIF5A2 on chemotherapy resistance in oral cancer cells in vitro. Methods. By using a lentiviral system, we investigated the effects of targeting EIF5A2 on the invasion, migration, growth, and chemosensitivity of SCC-9 cells to CDDP in vitro. Through the method of gene intervention, we explore the role of pro-apoptotic Bim and epithelial and mesenchymal marker E-cadherin protein in this process and the regulation of EIF5A2 on Bim and E-cadherin. Results. Targeting EIF5A2 reduces invasion and migration in SCC-9 cells partly through upregulation of E-cadherin expression; Targeting EIF5A2 promotes cell apoptosis and inhibits cell survival as well as increasing chemosensitivity in SCC-9 cells through upregulation of Bim expression. Conclusion. EIF5A2 may be a novel potential therapeutic target for oral cancer by upregulation of Bim and E-cadherin
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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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    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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    E2F1-EP300 co-activator complex potentiates immune escape in nasopharyngeal carcinoma through the mediation of MELK
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Wang, Qiang; Yu, Qi; Liu, Yueyang
    Background. Nasopharyngeal carcinoma (NPC) is characterized by a highly suppressive microenvironment that protects tumor cells against immune attack and facilitates tumor progression. MELK is upregulated in various tumors, whereas its function in the immune escape remains largely unknown. In this study, we investigated the role of MELK during immune escape in NPC. Methods. Differentially expressed genes were filtered using GEO datasets and PPI network analysis. NPC cell colony formation and motility were examined, and the impact of CD8+ T cells on NPC cells was evaluated. A xenograft model was constructed to detect the growth of tumor cells and the T-cell phenotype of tumor infiltration. ChIP-qPCR and dual-luciferase assays were used to verify the transcriptional regulation of MELK by EP300/E2F1. Findings. MELK was overexpressed in NPC, and sh-MELK suppressed the clonogenic ability, migration, and invasion of NPC cells and promoted the killing effects of CD8+ T cells. These in vitro findings were reproduced in vivo. EP300 synergized E2F1 to regulate the transcription of MELK in NPC cells. Loss of EP300 or E2F1 reverted the malignant phenotype of NPC cells and promoted the immune effect of CD8+ T cells. MELK further suppressed the immune effect of CD8+ T cells in the presence of sh-E2F1. Interpretation. EP300 coordinated with E2F1 to promote the transcription of MELK which promoted the growth of NPC cells and repressed the killing effect of CD8+ T cells. Blockage of MELK may be a potential way to suppress the immune escape of NPC cells.