Histology and histopathology Vol.39, nº4 (2024)
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- PublicationOpen AccessmiR-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, HuizhuanBackground. 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
- PublicationOpen AccessCold-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, AlfredoPrimary 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.
- PublicationOpen AccessEstradiol-mediated modulation of memory and of the underlying dendritic spine plasticity through the life span(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) González Burgos, Ignacio; Velázquez Zamora, Dulce A.; González Tapia, DavidThe morphophysiology of the nervous system changes and adapts in response to external environmental inputs and the experiences of individuals throughout their lives. Other changes in the organisms internal environment can also contribute to nervous system restructuring in the form of plastic changes that underlie its capacity to adapt to emerging psycho-physiological conditions. These adaptive processes lead to subtle modifications of the organisms internal homeostasis which is closely related with the activity of chemical messengers, such as neurotransmitters and hormones. Hormones reach the brain through the bloodstream, where they activate specific receptors through which certain biochemical, physiological, and morphological changes take place in numerous regions. Fetal development, infancy, puberty, and adulthood are all periods of substantial hormone-mediated brain remodeling in both males and females. Adulthood, specifically, is associated with a broad range of life events, including reproductive cycles in both sexes, and pregnancy and menopause in women. Events of this kind occur concomitantly with eventual modifications in behavioral performance and, especially, in cognitive abilities like learning and memory that underlie, at least in part, plastic changes in the dendritic spines of the neuronal cells in cerebral areas involved in processing cognitive information. Estrogens form a family that consists of three molecules [17β-estradiol (E2), estrone, estriol] which are deeply involved in regulating numerous bodily functions in different stages of the life-cycle, including the modulation of cognitive performance. This review addresses the effects of E2 on the dendritic spine-mediated synaptic organization of cognitive performance throughout the life span.
- PublicationOpen AccessTargeting 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, PengBackground 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
- PublicationOpen AccessTRIM11 expression in non-small cell lung cancer is associated with poor prognosis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Kuempers, Christiane; Jagomast, Tobias; Paulsen, Finn Ole; Heidel, Carsten; Bohnet, Sabine; Schierholz, Stefanie; Reischl, Markus; Dreyer, Eva; Olchers, Till; Reck, Martin; Kirfel, Jutta; Perner, SvenBackground. Despite promising results of targeted therapy approaches, non-small cell lung cancer (NSCLC) remains the leading cause of cancer-related death. Tripartite motif containing 11 (TRIM11) is part of the TRIM family of proteins, playing crucial roles in tumor progression. TRIM11 serves as an oncogene in various cancer types and has been reported to be associated with a poor prognosis. In this study, we aimed to investigate the protein expression of TRIM11 in a large NSCLC cohort and to correlate its expression with comprehensive clinico-pathological data. Methods. Immunohistochemical staining of TRIM11 was performed on a European cohort of NSCLC patients (n=275) including 224 adenocarcinomas and 51 squamous cell carcinomas. Protein expression was categorized according to staining intensity as absent, low, moderate and high. To dichotomize samples, absent and low expression was defined as weak and moderate and high expression was defined as high. Results were correlated with clinico-pathological data. Results. TRIM11 was significantly more highly expressed in NSCLC than in normal lung tissue and significantly more highly expressed in squamous cell carcinomas than in adenocarcinomas. We found a significantly worse 5-year overall survival for patients who highly expressed TRIM11 in NSCLC. Conclusions. High TRIM11 expression is linked with a poor prognosis and might serve as a promising novel prognostic biomarker for NSCLC. Its assessment could be implemented in future routine diagnostic workup.
- PublicationOpen AccessOncogenic 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, QinglinBackground. 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.
- PublicationOpen AccessE2F1-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, YueyangBackground. 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.
- PublicationOpen AccessDifferences in neuromuscular junctions between intrinsic muscles of the forepaw and biceps muscles in rats(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Qiao, Jing; Gu, Jing Yu; Li, BoMotor endplates of the interossei muscles become destabilized, whereas those of the biceps muscles remain stable in a rat model of obstetric brachial plexus palsy. However, it is unclear whether the morphology of the motor endplates of the interossei muscles is different from that of the biceps muscles in normal rat. We hypothesized that the motor endplates in the interossei muscles have specific characteristics different from those in the biceps muscles. The motor endplates were labeled with α-bungarotoxin and synaptophysin. The cross-sectional areas of the muscle fibers, the morphologies of the motor endplates, and the absolute and normalized areas (corrected by muscle fiber diameter) of the motor endplates of the interossei muscles and the biceps muscles were compared in rats at 1, 3, and 5 weeks after birth. The cross-sectional area of the interossei muscles and biceps muscle fibers were found to have increased gradually at 1, 3, and 5 weeks, but that of the biceps muscles was larger than that of the interossei muscles. The motor endplates of the interossei muscles and the biceps muscles gradually develop from crescent to pretzel shape after birth, and those of the interossei muscles have a smaller area. At 1, 3, and 5 weeks postnatally, the area of postnatal normalized motor endplates of the interossei muscles was much smaller than that of the biceps muscles. A better understanding of the morphological differences of the motor endplates between the interossei muscles and the biceps muscles may help to understand their physiological and pathological changes.
- PublicationOpen AccessThe emerging role of DOT1L in cell proliferation and differentiation: Friend or foe(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2024) Wu, Di; Zhang, Jing; Jun, Yang; Liu, Li; Huang, Cuiyuan; Wang, Wei; Yang, Chaojun; Xiang, Zujin; Wu, Jingyi; Huang, Yifan; Meng, Di; Yang, Zishu; Zhou, Xiaoyan; Cheng, Chen; Yang, JianCell proliferation and differentiation are the basic physiological activities of cells. Mistakes in these processes may affect cell survival, or cause cell cycle dysregulation, such as tumorigenesis, birth defects and degenerative diseases. In recent years, it has been found that histone methyltransferase DOT1L is the only H3 lysine 79 methyltransferase, which plays an important role in the process of cell fate determination through monomethylation, dimethylation and trimethylation of H3K79. DOT1L has a pro-proliferative effect in leukemia cells; however, loss of heart-specific DOT1L leads to increased proliferation of cardiac tissue. Additionally, DOT1L has carcinogenic or tumor suppressive effects in different neoplasms. At present, some DOT1L inhibitors for the treatment of MLL-driven leukemia have achieved promising results in clinical trials, but completely blocking DOT1L will also bring some side effects. Thus, this uncertainty suggests that DOT1L has a unique function in cell physiology. In this review, we summarize the primary findings of DOT1L in regulating cell proliferation and differentiation. Correlations between DOT1L and cell fate specification might suggest DOT1L as a therapeutic target for diseases.
- PublicationOpen AccessSystematic 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, JunBackground. 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.
- PublicationOpen AccessmicroRNA-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, LianObjective. 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.