Histology and histopathology Vol.37, nº4 (2022)
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- PublicationOpen AccessKnockdown of circular RNA hsa_circ_0062270 suppresses the progression of melanoma via downregulation of CDC45(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Hao, Tian; Yang, Yi; He, Juan; Bai, Jia; Zheng, Yongjian; Luo, ZhanpengBackground. Although systemic therapies for melanoma have been improved, the 5-year survival rate of this aggressive cancer remains poor. It has been shown that hsa_circ_0062270 was upregulated in patients with melanoma. However, the relevant mechanism of hsa_circ_0062270 in the progression of melanoma remains unclear. Methods. The CCK-8, EdU staining, flow cytometry, and transwell assays were used to determine the viability, proliferation, apoptosis and invasion in melanoma cells. An in vivo animal study was performed finally. Results. The level of hsa_circ_0062270 was significantly upregulated in melanoma cells. In addition, hsa_circ_0062270 knockdown markedly inhibited the viability, proliferation, invasion and promoted the apoptosis of melanoma cells. Cell division cycle protein 45 (CDC45) is the host gene of hsa_circ_0062270, and downregulation of hsa_circ_0062270 notably decreased the expression of CDC45 in melanoma cells. Rescue assays confirmed that hsa_circ_0062270 regulated the growth of melanoma cells through CDC45. Moreover, immunoprecipitation (RIP) analysis showed that hsa_circ_0062270 interacted with RNA-binding protein (RBP) EIF4A3. Furthermore, in vivo study indicated that knockdown of hsa_circ_0062270 inhibited the melanoma tumor growth in vivo. Conclusions. Downregulation of hsa_circ_0062270 can inhibit the progression of melanoma through downregulation of CDC45. Our findings provide biological mechanisms for the use of hsa_circ_0062270 as a biomarker for melanoma and potential therapeutic target.
- PublicationOpen AccessA review of neoplasms with MITF/MiT family translocations(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Wei, Shuanzeng; Testa, Joseph R.; Argani, PedramMicrophthalmia-associated transcription factor (MITF/MiT) family is a group of basic helix-loophelix leucine zipper (bHLH-LZ) transcription factors including TFE3 (TFEA), TFEB, TFEC and MITF. The first described neoplasms involving MITF family translocation were renal cell carcinomas with chromosome translocations involving ASPLTFE3/t(X;17)(p11.23;q25) or MALAT1-TFEB/t(6;11) (p21.1;q12), and now it is known as MiT family translocation RCC in 2016 WHO classification. Translocations involving MITF family genes also are found in other tumor types, such as perivascular epithelioid cell neoplasm (PEComa), alveolar soft part sarcoma (ASPS), epithelioid hemangioendothelioma, ossifying fibromyxoid tumor (OFMT), and clear cell tumor with melanocytic differentiation and ACTINMITF translocation. In this review, we summarize the features of different types of neoplasms with MITF family translocations.
- PublicationOpen AccessExpression of CXCL12 in esophageal high grade dysplasia characterized pathologically by lymphocyte accumulation directly under the lesion(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Mochizuki, Kunio; Oishi, Naoki; Odate, Toru; Tahara, Ippei; Inoue, Tomohiro; Kasai, Kazunari; Kondo, TetsuoSquamous dysplasia of the esophagus is an unequivocal neoplastic alteration of the esophageal squamous epithelium without invasion. Esophageal high grade dysplasia (EHGD) is characterized by >50% epithelial involvement or severe cytological atypia. Frequently, lymphocytes accumulate below EHGD lesions even though there is no invasion. If this lymphocytic accumulation is active, a transmitter should exist between the EHGD cells and the lymphocytes. CX-C motif chemokine ligand (CXCL) 12, CXCL10 and C-C motif chemokine ligand 18 (CCL18) are all lymphocyte chemoattractants in vivo, but there are no reports on the relationship between these chemokines and EHGDs. In this study, we investigated these chemokines and C-X-C motif chemokine receptor 4 (CXCR4) (receptor for CXCL12) in 30 EHGDs using immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR). For comparison, we enrolled 30 samples of normal esophageal squamous epithelium (NESE). We confirmed CXCL12 expression (H-score≥50 points) in 70% of EHGD and 0% of NESE samples, CXCL10 expression in 3% of EHGD and 3% of NESE samples, CCL18 expression in 3% of EHGD and 0% of NESE samples, and CXCR4 expression in 53% of EHGD and 0% of NESE samples by immunohistochemistry. EHGD and NESE cases were significantly different in their expressions between the tissue types (CXCL12, p<0.001; CXCR4, p<0.001). We examined CXCL12 and CXCR4 mRNA expressions of 3 representative EHGD samples, each having their respective immunostained areas detected by RT-PCR. Finding CXCL12 expression may indicate that this chemokine plays a part in the lymphocyte accumulation that occurs directly under EHGDs.
- PublicationOpen AccessDistal villous lesions are clinically more relevant than proximal large muscular vessel lesions of placental fetal vascular malperfusion(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Stanek, JerzyBackground. Fetal vascular malperfusion (FVM) can be diagnosed on placental examination based on histology of distal placental villi and large muscular placental vessels. While histology of both those placental compartments can be low grade or high grade, it is not known if these are clinically equivalent. This retrospective study aimed to compare the impact of placental distal villous and large vessel FVM lesions on clinical and placental phenotypes. Methods. Clinical and placental phenotypes of 479 consecutive ≥20 weeks of gestation at delivery cases of placental FVM were analyzed among 3 groups: Group 1: 86 cases with distal FVM (clusters of sclerotic distal villi and/or those with stromal vascular karyorrhexis and/or mineralization, and/or endothelial fragmentation by CD34 immunostain) without large vessel lesions; Group 2: 186 cases with large vessel lesions (fetal vascular ectasia, vascular thrombi, stem vessel obliteration, intramural fibrin deposition) without distal villous lesions; and Group 3: 207 cases showing both distal villous lesions and large fetal vessel lesions. Results. Statistically significant differences (Bonferroni correction) were observed in: average gestational age at delivery 31, 35, 34 weeks, fetal growth restriction 24, 9, 25%, average placental weight 318, 413, 366 g, postuterine pattern of chronic hypoxic placental injury 12, 2, 6%, luminal vascular abnormalities in stem vessels 16, 3, 11%, and high grade FVM 33, 16, 39%, among Groups 1-3, respectively. Conclusion. Because of longer time needed for its development, distal FVM portends poorer prognosis for the fetus than large vessel FVM
- PublicationOpen AccessTargeting AURKA by microRNA-490-3p suppresses gastric cancer cell growth(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Chen, Rui; Zhou, Shenkang; Fang, Chengfeng; Ye, Feifei; Chen, Jianhui; Jiang, PinluObjective. To illustrate the molecular mechanism of microRNA-490-3p regulating gastric cancer (GC) cells by targeting AURKA. Methods. Genes with significantly different expression in GC and normal tissue in TCGA-STAD dataset were analyzed by bioinformatics. Expression levels of genes and proteins in GC cells were measured by qRT-PCR and western blot. The interaction between microRNA-490-3p and AURKA was verified by dual luciferase assay. Proliferation, migration, invasion and apoptosis of GC cells were evaluated through a set of cell function assays. Results. MicroRNA-490-3p was significantly less expressed in GC, while AURKA was significantly highly expressed. Dual luciferase reporter gene assay proved that microRNA-490-3p targeted AURKA. Upregulation of microRNA-490-3p restrained proliferation, migration, invasion and stimulated apoptosis of GC cells, which was attenuated by overexpression of AURKA. Conclusions. MicroRNA-490-3p was likely to restrain the development of GC cells by inhibiting AURKA, and it may be an underlying target for GC treatment
- PublicationOpen AccessThe role of KMT2 gene in human tumors(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Zhang, Zhi Long; Yu, Peng Fei; Ling, Zhi QiangHistone methylation plays a crucial role in the regulation of gene transcriptional expression, and aberration of methylation-modifying enzyme genes can lead to a variety of genetic diseases, including human cancers. The histone modified protein KMT2 (lysin methyltransferase) family are involved in cell proliferation, growth, development and differentiation through regulating gene expression, and are closely related with many blood cancers and solid tumors. In recent years, several studies have shown that mutations in the KMT2 gene occur frequently in a variety of human cancers and the mutation status of the KMT2 gene may be correlated with the occurrence, development and prognosis of some tumors. Research uncovering the clinical characteristics and molecular mechanisms of KMT2 mutation in human tumors will be helpful for early diagnosis and prognosis of tumors as well as drug development for targeted therapies.
- PublicationOpen AccessCircular RNA circFADS2 inhibits the progression of cutaneous squamous cell carcinoma by regulating miR-766-3p/HOXA9 axis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Zhang, Zhang; Sun, Huijun; Hou, Junzhi; Lili Li, Lili Li; Wu, LijuanBackground. Mounting evidence indicates that circular RNAs (circRNAs) play vital roles in human diseases, especially in cancers. However, the biological functions and underlying mechanism of circRNA fatty acid desaturase 2 (circFADS2) in cutaneous squamous cell carcinoma (CSCC) have not been reported. Methods. The expression levels of circFADS2, microRNA-766-3p (miR-766-3p) and homeobox A9 (HOXA9) were determined by quantitative real-time PCR (qRT-PCR). Flow cytometry analysis was used to determine cell cycle distribution. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8) and colony formation assays. Wound healing and transwell assays were used to assess cell migration and invasion abilities. Glycolysis was examined via the measurement of extracellular acidification rate (ECAR). All protein levels were detected by western blot assay. The interaction between miR-766-3p and circFADS2 or HOXA9 was predicted by bioinformatics software and confirmed by dual-luciferase reporter, RNA pull-down, and RNA Immunoprecipitation (RIP) assays. The mouse xenograft model was established to investigate the role of circFADS2 in vivo. Results. CircFADS2 was downregulated in CSCC tissues and cells. CircFADS2 overexpression inhibited CSCC cell proliferation, metastasis and glycolysis. Moreover, miR-766-3p was able to directly bind to circFADS2, and circFADS2 played an anti-cancer role in CSCC by downregulating miR-766-3p. In addition, HOXA9 was a direct target of miR-766-3p, and miR766-3p inhibition suppressed CSCC cell proliferation, metastasis and glycolysis by upregulating HOXA9. Furthermore, circFADS2 acted as a sponge of miR-766- 3p to regulate HOXA9 expression. Besides, circFADS2 suppressed tumor growth in vivo. Conclusion. CircFADS2 suppressed CSCC progression by regulating miR-766-3p/HOXA9 axis, which might provide a promising therapeutic target for CSCC
- PublicationOpen AccessEnvironmental enrichment preserves hippocampal neurons in diabetes and stressed rats(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Pamidi, N.; Yap, C.G.; Nayak, S.This study evaluated the effect of Environmental Enrichment (EE) on neuron morphology in the CA1, CA3 and dentate hilus (DH) regions of the hippocampus by quantitating the total dendritic arborizations. EE is a potential intervention for stress and diabetes. It is capable of mitigating diabetes and stress-induced cognitive and memory deficit. Diabetes and stress were induced in male Wistar rats (4-5 weeks). Diabetic and stressed rats were exposed to EE on Day 2 post STZ injection and subsequently once daily for 30 days. All animals were sacrificed on Day 30. The hippocampus was dissected and processed for Golgi staining to quantitate dendritic arborizations at the CA1, CA2 and DH regions. Diabetes (D) and Diabetes+stress (D+S) groups had significantly fewer apical and basal dendritic branching points (ADBP, BDBP) at CA1 (p<0.01), CA3 (p<0.001) and DH (p<0.001) relative to control group (NC). Diabetes and stressed rats exposed to EE: [D+EE and D+S+EE groups] exhibited significantly denser ADBP and BDBP at all regions relative to D (p<0.001) and (D+S+EE) (p<0.001) groups respectively. EE significantly preserved neuronal arborizations in hippocampus of diabetic and stressed rats, suggesting a potential entity of diabetes and stress management.
- PublicationOpen AccessHigh miR-3648 expression and low APC2 expression are associated with shorter survival and tumor progression in NSCLC(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Dong, Yongquan; Wu, Biao; Wang, Xiongxiong; Lu, Feijie; Li, Qianjun; Zhao, QiongBackground. Emerging studies have demonstrated that microRNAs (miRNAs) play crucial roles in the carcinogenesis of many developing human tumors. However, the clinical significance and biological function of microRNA-3648 (miR-3648) in non-small cell lung cancer (NSCLC) have been largely undefined. Methods. The expression of miR-3648 and the mRNA of adenomatous polyposis coli 2 (APC2) in NSCLC tissues and cell lines were analyzed using quantitative real-time RT-PCR. The prognostic value of miR-3648 and APC2 was examined using the KaplanMeier method and Cox regression analyses. Experiments using NSCLC cells were conducted to explore the influences of miR-3648 on tumor cell proliferation, migration and invasion. Result. Increased expression of miR-3648 was observed in NSCLC tissues and cell lines compared with the corresponding controls (all P<0.05). miR-3648 expression was associated with the differentiation, lymph node metastasis and TNM stage (all P<0.05) of NSCLC patients, and high expression of miR-3648 was associated with poor overall survival rate. NSCLC cell proliferation, migration and invasion were significantly enhanced by miR-3648 overexpression. The further luciferase reporter assay and expression results showed that the decreased APC2 might also be a prognostic biomarker, and served as a target of miR-3648 in NSCLC. Conclusion. The findings from the present study indicate that the overexpression of miR-3648 serves as a useful biomarker for the prediction of prognosis in NSCLC, and promotes tumor cell proliferation, migration and invasion. APC2, as another prognosisrelated molecule, may be a target of miR-3648 in NSCLC.