Acta Universitatis Medicinalis Anhui

Journal Information

Superintend by

Anhui Provincial Education Department

Sponsored by

Anhui Medical University

Editor-in-chief

Weng Jianping

Edited and Published by

Editorial Board of Acta Universitatis Medi-cinalis Anhui Meishan Road , Hefei 230032

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Anhui Lianzhong Printing Limited

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Local Post Office , China

Domestic Distribution

Hefei Post Office of Anhui Province, China

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26 - 36

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China International Book Trading

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No.35, chegongzhuang West Road, Haidian District, Beijing, 100048,

China Code No . MO5933

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￥:10.00/Issue, 120.00/Year

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ISSN 1000 - 1492

CN 34 - 1065/R

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(0551)65161103, 65161192

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aydxb@vip.163.com (Submission)

aydxbsg@163.com (Review)

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AYDXAG

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The expression and function of MST1 in prostate cancer

Huang Yuhang； Yin Shiyuan； Fang Linna； Zhong Kun； He Guifang； Cai Yongping； Yin Yu

DOI: 专辑：医药卫生科技

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The mechanism of magnoflorine in inhibiting colon cancer based on network pharmacology andin vitroexperiment

Tan Lulu； Zhu Lina； Zhang Shujin； Wang Yuxuan； Li Huimei； Wang Yuke； Hou Jiayi； Feng Qilong ；Shi Jianyun

DOI: 专辑：医药卫生科技

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Advances in molecular mechanisms underlying the promotion of cancer development and progression by EphA2

Yu Hui； Han Chen； Wang Shili； Yang Haihong； Lu Peiyuan

DOI: 专辑：医药卫生科技

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Application value of deep learning reconstruction technology in enhancing the imaging efficiency and quality of HASTE and DWI sequences for liver MRI

Feng Lulu； Pan Zhili； Zhao Yingming

DOI: 专辑：医药卫生科技

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PRMT5 promotes angiogenesis in colorectal cancer via the JAK2/STAT3 signaling pathway

Zhang Wen; Geng Yongyong; Tu Xijiang; Yao Qianhui; Guo Wenlong; Yao Bogang; Sun Xuling

DOI: 专辑：医药卫生科技

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Abstract:
Objective To investigate the effect of protein arginine methyltransferase 5 (PRMT5) on the angiogenesis of colorectal cancer (CRC) through the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway. MethodsThe expression and prognostic value of PRMT5 in CRC tissues were analyzed based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. A total of 105 pairs of cancer tissues and matched adjacent non-tumor tissues were collected from CRC patients, and PRMT5 expression was detected by immunohistochemistry (IHC); Western blot was used to detect the PRMT5 protein level in normal colonic epithelial cells (FHC) and CRC cell lines (including RKO, SW480). SW48 and LoVo cells were divided into negative control (NC) group and PRMT5 knockdown interference group. After the stable knockdown cell models were successfully constructed, the effects of conditioned medium on the proliferation, cell cycle, migration and tube formation abilities of human umbilical vein endothelial cells (HUVECs) were detected; The correlation between PRMT5 and vascular endothelial growth factor A (VEGFA) was analyzed by real-time quantitative polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA). Gene set enrichment analysis (GSEA) and cytoplasm-nucleus separation assay were performed to verify the regulatory pathway. ResultsPRMT5 was highly expressed in CRC tissues and cell lines, which was significantly correlated with poor prognosis and pathological characteristics of patients (all P < 0.05); PRMT5 knockdown could significantly inhibit the angiogenesis-related abilities of HUVECs (all P < 0.05) and down-regulate the expression of VEGFA (all P < 0.01). GSEA results indicated that PRMT5 expression was significantly associated with the activation of JAK2/STAT3 signaling pathway (all P < 0.001). PRMT5 knockdown could inhibit the activation of JAK2/STAT3, the nuclear translocation of STAT3 and the protein level of phosphorylated STAT3 (p-STAT3) in the nucleus, thus inhibiting the expression of VEGFA. Conclusion PRMT5 is highly expressed in CRC tissues and indicates poor prognosis of patients. It promotes the nuclear translocation and transcriptional activity of STAT3 by activating the JAK2/STAT3 pathway and drives the expression of VEGFA to promote tumor angiogenesis.

Relationship between EDNRA gene polymorphisms and congenital bilateral absence of the vas deferens in the male Han Chinese population

Peng Yuwan1, He Xiaojin2 , Yang Xiaoyu3, Wang Jing4, Wang Binbin 4, Tang Dongdong5, Wei Zhaolian5, Cao Yunxia5

DOI: 专辑：医药卫生科技

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The change of EPA1-ROS-NLRP1 signaling in CUMS-induced depression model mice

Tian Shuxiang; Liu Mengqing; Yang Han; Niu Mingguang; Yin Yanyan

DOI: 专辑：医药卫生科技

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Abstract:
Objective To investigate the expression changes of the Endophilin A1 (EPA1)-ROS-NLRP1 signaling pathway in chronic unpredictable mild stress (CUMS)-induced depression model mice. MethodsC57BL/6 mice were randomly divided into control group and CUMS model group. The model mice received 42 days of CUMS stress exposure, after which behavioral changes were assessed through monitoring body weight, sucrose preference test, forced swim test, tail suspension test, open field test, and elevated plus-maze test. Hematoxylin-Eosin and Nissl staining were used to observe neuronal damage in hippocampal CA1 and CA3 regions. Calcium ion (Ca²⁺) assay kit was used to detect Ca²⁺ levels in the hippocampus. Immunofluorescence was used to detect colocalization of EPA1 and NLRP1 as well as ROS changes in the hippocampus. Transmission electron microscopy was used to observe mitochondrial structure in hippocampal neurons. The expression levels of calcium-activated neutral protease 1 (Calpain 1), nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2), NLRP1 inflammasome, downstream inflammatory proteins, and synapse-associated proteins in the hippocampus of mice was detected by using Western blot. Results Compared with the control group, mice in the CUMS model group exhibited depressive-like behavior and hippocampal neuronal damage. The levels of NLRP1 and EPA1 significantly increased in the hippocampus, and both were co-expressed in the cytoplasm and membrane of hippocampal neurons in the CUMS group mice（ P<0.01）. Ca²⁺ concentration was elevated（ P<0.01）, and the protein levels of Calpain 1 and NOX2 were upregulated（ P<0.01）. The average fluorescence intensity of ROS significantly increased, accompanied by structural damage to neuronal mitochondria（ P<0.01）; The levels of NLRP1 and its downstream inflammatory proteins significantly increased ( P<0.01), while the expression levels of synapse-associated proteins significantly decreased ( P<0.01). Conclusion EPA1 exhibits abnormal expression changes in CUMS-induced depression model mice, which may be closely associated with ROS generation, NLRP1 inflammasome activation, and the regulation of synaptic protein expression.

Research on the role of 7-dehydrocholesterol reductase in promoting the proliferation, migration, and invasion of lung adenocarcinoma cells

Tang Jing; Qiu Ping; Chen Renjie; Liu Yaqing; Liu Hui; Liu Yu; Chen Liwen

DOI: 专辑：医药卫生科技

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Abstract:
ObjectiveTo investigate the effects of 7-dehydrocholesterol reductase (DHCR7) in promoting proliferation, migration, and invasion of lung adenocarcinoma cells and the underlying signaling mechanisms. Methods The expression level of DHCR7 in lung adenocarcinoma and its prognosis were analyzed by using public databases. DHCR7 protein expression levels in the lung adenocarcinoma cell lines H1299 and A549 were assessed by Western blot, using the normal lung epithelial cell line BEAS-2B as a control. Small interfering RNA (siRNA) was used to knock down DHCR7 expression in H1299 and A549 cells. Assays including colony formation, CCK-8, wound healing, and Transwell experiments were conducted to assess the proliferation, migration, and invasion of the knockdown cells. Next, Western blot was employed to assess the phosphorylation levels of key signaling molecules in the Phosphoinositide 3-kinase/Protein Kinase B (PI3K/AKT), Janus Kinase/Signal Transducer and Activator of Transcription 3 (JAK/STAT3),Mitogen-activated protein kinase/extracellular signal-regulated kinase pathway (MAPK/ERK) (p-AKT, p-STAT3, p-ERK). ResultsBioinformatics results indicated that both DHCR7 mRNA and protein were highly expressed in lung adenocarcinoma compared with normal tissues adjacent to cancer. Furthermore, higher DHCR7 mRNA level was associated with poor prognosis ( P< 0.001). The expression levels of DHCR7 were significantly higher in both H1299 and A549 cells than that in BEAS-2B cells ( P< 0.05, P< 0.01). Compared with si-Control, the proliferation, migration, and invasion abilities of si- DHCR7 H1299 and A549 cells significantly decreased. Among the phosphorylated signaling molecules detected, p-ERK was significantly downregulated ( P< 0.000 1, P< 0.01) whereas p-AKT and p-STAT3 levels were not significantly changed. ConclusionDHCR7 has prominent effects in promoting the proliferation, migration, and invasion of lung adenocarcinoma cells, and the underlying mechanisms are related to the MAPK/ERK signaling pathway.

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