Histology and histopathology Vol.37, nº9 (2022)
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- PublicationOpen AccessMiR-129-5p/TRIP13 affects malignant phenotypes of colorectal cancer cells(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Cao, Yongqing; Huang, Fang; Liu, Jiheng; Qi, Hui; Xiao, JinjunObjective. Aberrant miR-129-5p expression is a key modulator of cancer development. But how the miRNA affects colorectal cancer (CRC) remains unclear. This study was designed to illustrate the underlying mechanism of miR-129-5p in CRC. Methods. MiR-129-5p expression at cellular level was assayed by qRT-PCR. Its role in CRC cell phenotypes was studied by cell function experiments. The binding relationship between miR-129-5p and TRIP13 was analyzed and verified by bioinformatics prediction and dual-luciferase detection. Furthermore, the functional mechanism based on miR-129-5p and TRIP13 in CRC was studied through rescue experiments. Results. CRC cell lines presented prominently lower miR-129-5p levels than the normal colon epithelial cell line. The forced miR-129-5p level suppressed CRC cell growth. TRIP13 was proved to be a target of miR-129- 5p in CRC cells, and miR-129-5p overexpression reduced TRIP13 expression. TRIP13 knockdown resulted in cell cycle arrest. Additionally, TRIP13 overexpression restored the impacts of miR-129-5p overexpression on cell malignant phenotypes and cell cycle. Conclusion. MiR-129-5p down-regulated TRIP13 expression, thereby restraining the malignant progression of CRC cells. The findings may offer a new target for molecular therapy of CRC.
- PublicationOpen AccessCircRNA circBACH1 facilitates hepatitis B virus replication and hepatoma development by regulating the miR-200a-3p/MAP3K2 axis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Du, Na; Li, Kailin; Wang, Yu; Song, Bo; Zhou, Xuan; Duan, ShaoqiongBackground. Hepatitis B virus (HBV) is a top contributor to hepatoma. Circular RNAs (circRNAs) have been elucidated to have a close connection with HBV-induced hepatoma. This study aimed to explore the role of circRNA BTB domain and CNC homolog 1 (circBACH1) in HBV replication and hepatoma progression, as well as the potential mechanistic pathway. Methods. Quantitative real-time polymerase chain reaction (qRT-PCR) assay was performed to assess the expression of circBACH1, microRNA (miR)-200a-3p, and mitogen-activated protein kinase kinase kinase 2 (MAP3K2). HBV replication was determined by enzyme-linked immunosorbent assay (ELISA) and qRTPCR assay. Cell viability and clonogenicity were detected via Cell Counting Kit-8 (CCK-8) assay and colony formation assay, respectively. Cell metastasis was examined by Transwell assay and wound healing assay. Annexing-V/PI staining was employed to monitor cell apoptosis using flow cytometry. Levels of MAP3K2, proliferation- and apoptosis-related proteins were analyzed by Western blotting. Target interaction between miR-200a-3p and circBACH1 or MAP3K2 was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The role of circBACH1 in vivo was investigated by xenograft model assay. Results. Expression of circBACH1 and MAP3K2 was increased, while miR-200a-3p expression was decreased in HCC tissues and HBV-transfected hepatoma cells. Depletion of circBACH1 or miR-200a3p overexpression impeded HBV replication, proliferation, and metastasis in HBV-transfected hepatoma cells. CircBACH1 was able to regulate MAP3K2 expression by sponging miR-200a-3p. CircBACH1 regulated HBV replication and hepatoma progression through the miR-200a-3p/MAP3K2 pathway. Moreover, circBACH1 deficiency hampered tumor growth in vivo. Conclusion. CircBACH1 knockdown had inhibitory effects on HBV replication and hepatoma progression, at least partly by modulating the miR-200a-3p/MAP3K2 axis
- PublicationOpen AccessCharacterization of diet based nonalcoholic fatty liver disease/nonalcoholic steatohepatitis in rodent models: Histological and biochemical outcomes(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Akbari, Ghaidafeh; Mard, Seyyed Ali; Savari, Feryal; Barati, Barat; Sameri, Maryam JafarNonalcoholic fatty liver disease (NAFLD), as the most common chronic liver disease, is rapidly increasing worldwide. This complex disorder can include simple liver steatosis to more serious stages of nonalcoholic fibrosis and steatohepatitis (NASH). One of the critical concerns in NASH research is selecting and confiding in relying on preclinical animal models and experimental methods that can accurately reflect the situation in human NASH. Recently, creating nutritional models of NASH with a closer dietary pattern in human has been providing reliable, simple, and reproducible tools that hope to create a better landscape for showing the recapitulation of disease pathophysiology. This review focuses on recent research on rodent models (mice, rats, and hamsters) in the induction of the dietary model of NAFLD /NASH. This research tries to compile the different dietary compositions of NASH, time frames required for disease development, and their impact on liver histological features as well as metabolic parameters.
- PublicationOpen AccessAADAC promotes therapeutic activity of cisplatin and imatinib against ovarian cancer cells(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Wang, Haijing; Wang, Disong; Gu, Tingting; Zhu, Mengjiao; Cheng, Ling; Da, WentaoObjective. To explore how AADAC functions in the malignant progression of ovarian cancer, and the effect of AADAC on drug therapeutic activity against ovarian cancer cells. Methods. AADAC level in tumor and normal samples from TCGA-OV dataset and its survival significance were analyzed by bioinformatics methods. Signaling pathway enrichment analysis for the high- and low-AADAC patients was achieved by using GSEA software. AADAC expression in the cell lines with different treatments was evaluated via qRT-PCR. Cell proliferative ability was assessed via MTT assay Cell migratory and invasive abilities were evaluated via transwell assay. Angiogenesis assay was performed to examine the angiogenetic ability. Results. AADAC was upregulated in ovarian cancer tissues, and patients with high expression of AADAC had favorable survival conditions compared to the low AADAC expression ones. Overexpression of AADAC inhibited the malignant progression of ovarian cancer cells. Both cisplatin and imatinib suppressed cancer cell malignant progression, while overexpressed AADAC synergistically enhanced such inhibition. Conclusions. The study demonstrated that AADAC could somehow suppress the malignant progression of ovarian cancer, especially at the cellular level. In addition, synergic tumor-inhibitory effects between AADAC and the anti-cancer drugs were identified. All the above results proposed a novel idea and candidate biomarker for ovarian cancer therapy.
- PublicationOpen AccessMiR-486-5p specifically suppresses SAPCD2 expression, which attenuates the aggressive phenotypes of lung adenocarcinoma cells(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Wei, Desheng. Background. MiR-486-5p expression is restrained in lung adenocarcinoma (LUAD). However, much less has been understood on its role in LUAD. We aimed to explore the biofunctions of miR-486-5p in LUAD. Methods. A differential expression analysis based on The Cancer Genome Atlas-LUAD dataset was done to screen the differently expressed miRNAs and mRNAs. MiR-486-5p and SAPCD2 mRNA expression was analyzed by qRT-PCR, and protein level of SAPCD2 was assayed by western blot. Upregulation and downregulation of miR-486-5p or SAPCD2 were achieved by cell transfection. For cell function assays, the proliferation of cancer cells was examined by MTT assay. Cell apoptosis was assessed by flow cytometry and microscopy. Transwell assay was applied to evaluate cell migration and invasion. A dual-luciferase detection was employed to determine the miRNA-mRNA targeting relationship. Results. MiR-486-5p expression was notably reduced in LUAD tissue and cell lines. Upregulating miR-486-5p restrained the anti-apoptotic and proliferative abilities, as well as cell migratory and invasive phenotypes in LUAD cells. SAPCD2 was determined as one target of miR-486-5p. Also, SAPCD2 forced expression was able to attenuate the inhibitory impacts of miR-486-5p on the malignant phenotypes of LUAD cells. Conclusion. MiR-486-5p suppressed cell malignant progression in LUAD by targeting SAPCD2, suggesting that the two may be targets for LUAD treatment.
- PublicationOpen AccessEPHB2 as a recurrence-related gene and a prognostic indicator in nasopharyngeal carcinoma: A bioinformatics screening and immunohistochemistry verification(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Ling, Junjun; Chang, Aoshuang; Zhao, Houyu; Ye, Huiping; Zhuo, XianluRecurrence and metastasis of nasopharyngeal carcinoma (NPC) after radical treatment is a major bottleneck in clinical treatment. Therefore, we aimed to find the genes related to metastasis after radical treatment in NPC patients. Public datasets in the Gene Expression Omnibus database were consulted and the differential expression genes (DEGs) were screened out. The possible roles of the DEGs were annotated by Gene Ontology, and pathway analysis. The hub genes/proteins were then filtered out through protein-protein interaction network construction. The key genes were sifted out from the hub genes, and their expressions were verified by qPCR and immunohistochemistry assays. A total of 28 DEGs were filtered out, which may be enriched in different signaling pathways. Of these DEGs, 11 hub genes were filtered out, among which EPHB2 was shown to be over-expressed in NPC tissues. Further experimental assays confirmed that EPHB2 was overexpressed in NPC cells, which might be associated with tumor recurrence, neck lymph node metastasis, and advanced clinical stages. Moreover, high EPHB2 expression predicted poor prognosis in NPC patients. EPHB2 might be a novel recurrence-related biomarker and a prognostic factor for NPC. Moreover, it might also be used as a potential treatment target for NPC.