Histology and histopathology Vol.39,nº10 (2024)
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- PublicationOpen AccessRNA-binding protein DND1 participates in migration, invasion, and EMT of prostate cancer cells by degrading CLIC4(Universidad de Murcia. Departamento de Biología Celular e Histología, 2024) Zhang, Wei; Xu, Qian; Shi, Chunmei; Chen, Xinfeng; Shen, Cheng; Zhang, Yong; Zheng, Bing; Zhu, HuaDead-End 1 (DND1) is an RNA-binding protein (RBP) with regulatory functions in multiple cancers, including gastric and colorectal. Nevertheless, the role that DND1 plays in prostatic cancer (PCa) as well as the hidden molecular mechanism is still obscure. The gene expression of DND1 and survival analyses in PCa were analyzed by the UALCAN database. Expression of DND1 and chloride intracellular channel 4 (CLIC4) were detected by qRT-PCR and western blot analysis. The Cell Counting Kit-8 assay and EDU staining were employed for the estimation of cell viability. The capabilities of cells to migrate and invade were appraised by the wound healing assay as well as the Transwell assay, while epithelial-mesenchymal transition (EMT) was measured by immunofluorescence and western blot assay. The interaction of DND1 and CLIC4 was predicted by PCTA, linkedomics, and RPISeq databases. It was discovered that DND1 expression was elevated in PCa cells. DND1 silencing had suppressive impacts on the proliferative, migrative, and invasive capabilities as well as EMT in DU145 and 22Rv1 cells. Mechanistically, bioinformatic analysis demonstrated that DND1 was negatively correlated with CLIC4 and that DND1 protein could bind to CLIC4 mRNA. Additionally, the CLIC4 level was reduced in PCa cells. CLIC4 depletion countervailed the suppressive impacts of DND1 deficiency on the capabilities of DU145 and 22Rv1 cells to proliferate, migrate, and invade as well as the process of EMT. These results suggested that DND1 silencing repressed the proliferation, migration, invasion, and EMT in PCa by regulating the mRNA level of CLIC4.
- PublicationOpen AccessThe potential of EZH2 expression to facilitate treatment choice in stage II colorectal adenocarcinoma(Universidad de Murcia. Departamento de Biología Celular e Histología, 2024) Zhu, Xiaoqun; He, Lu; Zheng, Zhong; Wang, Ya; Yang, Jun; Zhang, Biao; Wang, Chaoshan; Li, ZhiwenBackground. The current selection criteria of patients with stage II colorectal carcinoma (CRC) suitable for adjuvant therapy are not satisfactory. Enhancer of zeste homolog 2 (EZH2) has been demonstrated to be over-expressed in CRC. However, data regarding the role of EZH2 in CRC survival remains controversial, and little is known about it in stage II CRC. Thus, we conducted this study to investigate the clinical significance of EZH2 expression in stage II CRC. Methods. Cases with stage II CRC resected between 2015 and 2018 were retrospectively reviewed. EZH2 expression was analyzed by immunohistochemistry using tissue microarrays. The relationship between EZH2 expression and clinicopathological variables was analyzed. Survival curves were estimated by the KaplanMeier approach. Results. We found high EZH2 expression in 134 of 221 analyzable stage II tumors (60.63%). No significant associations were observed between EZH2 expression and common clinicopathological factors. Survival analyses showed that cases receiving surgery alone had inferior overall survival (OS) than those receiving surgery and chemotherapy (P=0.0075) in stage II CRC with high EZH2 expression, however, metastasis-free survival (MFS) was similar between these two subgroups. Treatment choice had no impact on the survival of stage II CRC with low EZH2 expression. Conclusion. The OS of stage II CRC with high EZH2 expression improved more strikingly with surgery and adjuvant chemotherapy than with surgery alone, which suggests the potential of EZH2 expression as a biomarker to help identify a subgroup of early-stage CRC benefiting from surgery and adjuvant chemotherapy. More large-scale studies are warranted to corroborate this finding and to further evaluate the predictive nature of EZH2.
- PublicationOpen AccessUpregulation of LY6K induced by FTO-mediated demethylation promotes the tumorigenesis and metastasis of oral squamous cell carcinoma via CAV-1-mediated ERK1/2 signaling activation(Universidad de Murcia. Departamento de Biología Celular e Histología, 2024) Xu, Chen; Gong, Rujuan; Yang, HaibingLymphocyte antigen 6 complex locus K (LY6K) has been demonstrated to play a significant role in cancers and identified as a therapeutic biomarker for head and neck squamous cell carcinoma. However, the role of LY6K in oral squamous cell carcinoma (OSCC) has not been explored. The current study discovered that LY6K was aberrantly upregulated in OSCC cell lines and tissues and that high LY6K expression significantly correlated with poorer survival of OSCC patients. Through stable knockdown of LY6K, we found that the growth, colony formation, migration, and invasion of OSCC cells were substantially suppressed. In addition, tumor growth and lung metastasis in vivo were effectively inhibited by LY6K depletion. Mechanically, LY6K binds with CAV-1 and activates CAV-1-mediated MAPK/ERK signaling to exert its oncogenic effects on OSCC. In addition, LY6K expression in OSCC was discovered to be regulated by FTO-mediated RNA N6- methyladenosine (m6A) modification in an IGF2BP1- dependent manner. Generally, LY6K expression was upregulated by FTO-mediated demethylation in OSCC, which promoted the tumorigenesis and metastasis of OSCC via activating the CAV-1-mediated ERK1/2 signaling pathway
- PublicationOpen AccessFunctional mechanism of baicalein in alleviating severe acute pancreatitis-acute lung injury by blocking the TLR4/MyD88/TRIF signaling pathway(Universidad de Murcia. Departamento de Biología Celular e Histología, 2024) Yang, Qingjing; Yue, Chao; Huang, Xing; Wang, Zihe; Li, Zhenlu; Hu, Weiming; Lu, Huiminy. Severe acute pancreatitis-acute lung injury (SAP-ALI) is a disease with high mortality. This study aims to explore the mechanism of baicalein on SAP-ALI in rats by blocking toll-like receptor-4 (TLR4)/myeloid differentiation primary response gene 88 (MyD88)/TIRdomain-containing adapter-inducing interferon-β (TRIF) signal pathway. The SAP-ALI rat model was established by intraperitoneal injection of 3% pentobarbital sodium (30 mg/kg), with pancreas and intestines turned over, injected with 3.5% sodium taurocholate backward into the bile-pancreatic duct at 0.1 mL/100 g for 12h, and treated with baicalein, lipopolysaccharide (LPS), miR182 agomir, or miR-182 antagomir. The TLR4/MyD88/ TRIF pathway was activated using LPS in SAP-ALI rats after baicalein treatment. Baicalein attenuated inflammatory cell infiltration, alveolar wall edema, decreased W/D ratio and levels of TLR4, MyD88, and TRIF in the lung tissues, reduced levels of inflammatory factors in pancreatic and lung tissues and BALF, diminished ROS, and elevated GSH, SOD and CAT in pancreatic and lung tissues of SAP-ALI rats. Activation of the TLR4/MyD88/TRIF pathway partly abrogated baicalein-mediated improvements in inflammation and oxidative stress in SAP-ALI rats. miR-182 targeted TLR4. miR-182 suppressed inflammation and oxidative stress in SAP-ALI rats by targeting TLR4. Inhibition of miR-182 partly nullified baicalein-mediated attenuation on inflammation and oxidative stress in SAP-ALI rats. In conclusion, baicalein can inhibit the TLR4/MyD88/ TRIF pathway and alleviate inflammatory response and oxidative stress in SAP-ALI rats by upregulating miR182 and suppressing TLR4, thus ameliorating SAP-ALI.
- PublicationOpen AccessColorectal cancer histopathology image analysis: A comparative study of prognostic values of automatically extracted morphometric nuclear features in multispectral and red-blue-green imagery(Universidad de Murcia. Departamento de Biología Celular e Histología, 2024) Liu, Wenlou; Qu, Aiping; Yuan, Jingping; Wang, Linwei; Chen, Jiamei; Zhang, Xiuli; Wang, Hongmei; Han, Zhengxiang; Li, Yan
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