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Long noncoding RNA LINC01106 promotes lung adenocarcinoma progression via upregulation of autophagy

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Oncology research 2025年第1期33卷 171-184页

作者： Gengyun Sun Yiping Zheng Jianfeng Cai Jie Gao Lie Dong Xiangbin Zhang Yinghui Huang department of respiratory and Critical Care medicine The First Affiliated Hospital of Anhui Medical University Hefei 230022 China. department of respiratory and Critical Care medicine Nanping First Hospital Affiliated to Fujian Medical University Nanping 353006 China.

Background:Long noncoding RNA, LINC01106 exhibits high expression in lung adenocarcinoma (LUAD) tumor tissues, but its functional role and regulatory mechanism in LUAD cells remain unclear.Methods:LINC01106 expression was analyzed in LUAD tissues and its functional impact on LUAD cells was assessed. LUAD cells were silenced with sh-LINC01106 and injected into nude mice to investigate tumor growth. The downstream transcription factors and molecular mechanism were determined using the Human transcription factor database (TFDB) database and Gene Expression Profiling Interactive Analysis (GEPIA) database. Additionally, the impact of linc01106 on autophagy was analyzed by determining the expression of autophagy-related genes (ATGs) in LUAD cells.Results:Our results showed that LINC01106 exhibited upregulation in both LUAD tissues and cell lines. The silencing of LINC01106 demonstrated a suppressive effect on tumorigenesis in a xenograft mouse model of LUAD. Additionally, LINC01106 was found to recruit TATA-binding protein-associated factor 15 (TAF15), an RNA-binding protein, thereby enhancing the mRNA stability of TEA domain transcription factor 4 (TEAD4). In turn, TEAD4 served as a transcription factor that bound to the LINC01106 promoter and regulated its expression. Further assays indicated that LINC01106 promoted autophagy in LUAD cells by upregulating the expression of autophagy-related genes (ATGs). The silencing of LINC01106 in LUAD cells inhibited autophagy, and cell proliferation, and promoted apoptosis, which all were effectively reversed by ATG5 overexpression.Conclusions:Overall, LINC01106, transcriptionally activated by TEAD4, interacts with TAF15 to promote the stability of TEAD4 and upregulates the expression of ATGs, promoting malignancy of LUAD cells.

关键词： ATG5 LINC01106 Lung adenocarcinoma (LUAD) Non-small cell lung cancer (NSCLC) TAF15 TEAD4

Disruption of neuronal actin barrier promotes the entry of disease-implicated proteins to exacerbate amyotrophic lateral sclerosis pathology

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Neural Regeneration Research 2025年第9期20卷 2589-2590页

作者： Mikio Shimizu Tatsusada Okuno department of Neurology Osaka University Graduate School of MedicineSuitaJapan department of Neurology Osaka General Medical CenterOsakaJapan

Amyotrophic lateral sclerosis(ALS)is a devastating neurological disease characterized by the accumulation of aberrant proteins in motor neurons of the brain and spinal *** with ALS develop skeletal muscle weakness,resulting in death from respiratory paralysis,which usually occurs 2-4 years after clinical onset(Goutman et al.,2022).

关键词： paralysis sclerosis

Effects of glucocorticoid and cysteinyl leukotriene 1 receptor antagonist on CD_(34)^+ hematopoietic cells in bone marrow of asthmatic mice

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Chinese Medical Journal 2004年第4期117卷 592-597页

作者：毛辉殷凯生王曾礼李富宇department of General Surgery West China Hospital 张希龙刘春涛雷松department of Tumor Biological Therapy West China Hospital department of respiratory medicine department of respiratory medicine West China Hospital

BACKGROUND: Corticosteroids remain the most effective therapy available for asthma. They have widespread effects on asthmatic airway inflammation. However, little is known about the effects of corticosteroids on the production of bone marrow inflammatory cells in asthma. This study observed the effects of glucocorticoid and cysteinyl leukotriene 1 receptor antagonist on CD34+ hematopoietic cells, so as to explore the possible effectiveness of a bone marrow-targeted anti-inflammatory strategy. METHODS: Balb/c mice were sensitized and challenged with ovalbumin (OVA) to establish an asthmatic model. For two consecutive weeks, asthmatic mice were challenged with OVA while being given either prednisone, montelukast, prednisone plus montelukast, or sterile saline solution. The mice were killed 24 hours after the last challenge with OVA, and bronchoalveolar lavage fluid (BALF), peripheral blood, and bone marrow were collected. Eosinophils in peripheral blood and BALF, and nucleated cells in BALF, peripheral blood, and bone marrow were counted. The percentages of CD34+ cells, CD4+ T lymphocytes and CD8+ T lymphocytes among nucleated cells in peripheral blood and bone marrow were counted by flow cytometry. Immunocytochemistry and in situ hybridization were employed to detect expression of CD34 and interleukin (IL)-5Ralpha mRNA (CD34+ IL-5Ralpha mRNA+ cells) among bone marrow hematopoietic cells. RESULTS: Compared with the sterile saline solution group, the number of eosinophils in BALF and peripheral blood, CD34+ cells in peripheral blood and bone marrow, and CD34+ IL-5Ralpha mRNA+ cells in bone marrow of mice from the prednisone and prednisone plus montelukast groups were significantly lower (P

关键词： Acetates Animals Antigens, CD34 Asthma Cell Count Hematopoietic Stem Cells Immunohistochemistry In Situ Hybridization Interleukin-5 Male Mice Mice, Inbred BALB C Prednisone Quinolines Research Support, Non-U.S. Gov't

Effect of Nuclear Factor-κB on Airway Remodeling in Asthmatic Rats

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2004年第1期24卷 13-18页

作者：许淑云徐永健张珍祥倪望陈士新 department of respiratory medicine

In order to investigate the effect of nuclear factor κB (NF κB) on airway remodeling in asthmatic rats, 18 Wistar rats were divided into three groups: asthmatic group; pyrrolidine dithiocarbamate (PDTC) group, in which rats were injected intraperitoneally with NF κB specific inhibitor PDTC (100 mg/kg) before ovalbumin (OVA) challenge; control group. The NF κB activity and the expression of inhibitory protein κBα (I κBα) in airway were detected by electrophoretic mobility shift assay (EMSA), Western blot and immunohistochemistry respectively. The infiltration of inflammatory cells, the number of Goblet cells, the area of collagen and smooth muscle in airway were measured by means of image analysis system. The results showed that with the up regulation of airway NF κB activity in asthmatic group, the number of goblet cells (3.08±0.86/100 μm basement membrane (BM)), the area of collagen (24.71±4.24 μm 2/μm BM) and smooth muscle (13.81±2.11 μm 2/μm BM) in airway were significantly increased ( P 0.05). It was concluded that the activity of NF κB is increased in airway of asthmatic rats. Inhibition of NF κB activation can attenuate constructional changes in asthma airway, suggesting NF κB may contribute to asthmatic airway remodeling.

关键词： asthma airway remodeling nuclear factor kappaB

Expression of P53,P21 in Human Lung Adenocarcinoma A549 Cell Strains under Hypoxia Conditions and the Effect of TSA on Their Expression

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2003年第4期23卷 359-361页

作者：黄宏张珍祥徐永健邵静芳 department of respiratory medicine

This paper was designed to investigate the expression of p53, p21of A549 cell strains under hypoxic condition and the effect of trichostatin A (TSA), the inhibitor of histone deacetylase1 (HDAC1) on their expression. The authors designed 1 normoxia group (control group) and 6 hypoxia groups (experiemntal group): hypoxia 6 h group (A), TSA+ hypoxia 6 h (B), hypoxia 12 h group (C) ,hypoxia 24 h group (D), TSA+hypoxia 24 h (E), hypoxia 48 h group (F). The expression of HDAC1 in A549 cells was examined by using Western blot and the expression of p53, p21 in A549 cells and the effect of TSA on them were determined by using immunohistochemistry and reverse transcription polymerase chain reaction (RT PCR). The A value expressed by HDAC1 in A549 cell strains was 138±11 in the control group, 78±4, 86±5, 124±3, 120±9 in experimental groups A, C, D, F, respectively. The A value of the expression of the protein and mRNA of p53 in A549 cell strains were 0.12±0.02, 0.62±0.02 in the control group, 0.10±0.03, 0.32±0.03; 0.11±0.01, 0.33±0.02; 0.13±0.03, 0.58±0.01; 0.12±0.02, 0.56±0.02 in experimental group A, B, D, E, respectively. The A value of the expression of the protein and mRNA of p21 in A549 cell strains were 0.17±0.03, 0.62±0.03 in the control group, 0.16±0.02, 0.50±0.02; 0.14±0.02, 0.36±0.02; 0.15±0.03, 0.49±0.03; 0.13±0.02, 0.33±0.02 in experimental groups A, B, D, E, respectively. These results indicate that the expression of HDAC1 is regulated by hypoxia and the effect of TSA is closely related to the expression of P21 under hypoxia condition.

关键词： p53 p21 histone deacetylase trichostain A hypoxia

Heat Shock Protein 70 Gene Polymorphisms in Han Nationality of China with Chronic Obstructive Pulmonary Diseases

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2004年第1期24卷 28-31页

作者：谢俊刚徐永键张珍祥倪望陈仕新 department of respiratory medicine

In order to investigate whether polymorphism in gene for heat shock protein 70 (HSP70) has any bearing on individual susceptibility to the development of chronic obstructive pulmonary disease(COPD), the geotypes of 88 patients with COPD and 87 healthy smoking control subjects were tested by polymerase chain reaction followed by restriction fragment polymorphism analysis for HSP70 gene. In COPD group, HSP70 1 genotype A/A, A/B and B/B was 59.1 %, 35.2 % and 5.7 %, HSP70 2 genotype A/A, A/B and B/B was 26.1 %, 54.6 % and 19.3 %, and HSP70 hom genotype A/A, A/B and B/B was 70.4 %, 27.3 % and 2.3 % respectively. In the control group, it was 60.9 %, 27.5 % and 3.5 %, 20.7 %, 56.3 % and 23.0 %, and 54.0 %, 42.5 % and 3.5 %, respectively. The frequency of polymorphic genetypes showed no difference between the COPD group and the control group ( P >0.05). It was suggested that geneic polymorphism in HSP70 is not associated with development of COPD in Han nationality of China.

关键词： lung disease, obstructive heat shock protein 70 smoking

Effect of Nuclear Factor-kappa B on Vascular Endothelial Growth Factor mRNA Expression of Human Pulmonary Artery Smooth Muscle Cells in Hypoxia

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2004年第1期24卷 9-12,18页

作者：张焕萍徐永健张珍祥许淑云倪望陈士新 department of respiratory medicine

In order to investigate the effect of nuclear factor kappa B (NF κB) on vascular endothelial growth factor (VEGF) mRNA expression of human pulmonary artery smooth muscle cells (HPASMCs) in hypoxia, the cultured HPASMCs in vitro were stimulated with pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF κB. The NF κB p65 nuclei positive expression was detected by immunocytochemical technique. The IκBα protein expression was measured by Western blot. RT PCR was used to detect the VEGF mRNA expression of HPASMCs. The results showed that no significant change was observed in the NF κB p65 nuclei positive expression of cultured HPASMCs during 6 h-24 h in normoxia, but the levels of NF κB p65 nuclei positive expression of cultured HPASMCs were significantly increased in hypoxia groups as compared with those in all normoxia groups ( P <0.05). The IκBα protein expression of cultured HPASMCs showed no significant change during 6 h-24 h in normoxia, but significantly decreased in hypoxia as comapred with that in normoxia groups ( P <0.05). PDTC (1 to 100 μmol/L) could inhibit the VEGF mRNA expression of HPASMCs in a concentration dependent manner in hypoxia. In conclusion, NF κB can be partly translocation activated from cytoplasm into nuclei in the cultured HPASMCs under hypoxia. The inhibition of NF κB activation can decrease the VEGF mRNA expression. It is suggested that the activation of NF κB is involved in the VEGF mRNA expression of HPASMCs under hypoxia.

关键词： hypoxia pulmonary artery smooth muscle vascular endothelial growth factor nuclear factor kappa B

Persistent alterations in gray matter in COVID-19 patients experiencing sleep disturbances:a 3-month longitudinal study

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Neural Regeneration Research 2025年第10期20卷 3013-3024页

作者： Kaixuan Zhou Gaoxiong Duan Ying Liu Bei Peng Xiaoyan Zhou Lixia Qin Lingyan Liang Yichen Wei Qingping Zhang Xiaocheng Li Haixia Qin Yinqi Lai Yian Lu Yan Zhang Jiazhu Huang Jinli Huang Yinfei Ouyang Bolin Bin Mingming Zhao Jun Liu Jianrong Yang Demao Deng Guangxi Key Laboratory of Special Biomedicine School of MedicineGuangxi UniversityNanningGuangxi Zhuang Autonomous RegionChina department of Radiology the People’s Hospital of Guangxi Zhuang Autonomous RegionGuangxi Academy of Medical SciencesNanningGuangxi Zhuang Autonomous RegionChina department of Sleep medicine the People’s Hospital of Guangxi Zhuang Autonomous RegionNanningGuangxi Zhuang Autonomous RegionChina department of Radiology The Second Xiangya HospitalCentral South UniversityChangshaHunan ProvinceChina Guangxi Clinical Research Center for Sleep medicine the People’s Hospital of Guangxi Zhuang Autonomous RegionNanningGuangxi Zhuang Autonomous RegionChina

Sleep disturbances are among the most prevalent neuropsychiatric symptoms in individuals who have recovered from severe acute respiratory syndrome coronavirus 2 *** studies have demonstrated abnormal brain structures in patients with sleep disturbances who have recovered from coronavirus disease 2019(COVID-19).However,neuroimaging studies on sleep disturbances caused by COVID-19 are scarce,and existing studies have primarily focused on the long-term effects of the virus,with minimal acute phase *** a result,little is known about the pathophysiology of sleep disturbances in the acute phase of *** address this issue,we designed a longitudinal study to investigate whether alterations in brain structure occur during the acute phase of infection,and verified the results using 3-month follow-up data.A total of 26 COVID-19 patients with sleep disturbances(aged 51.5±13.57 years,8 women and 18 men),27 COVID-19 patients without sleep disturbances(aged 47.33±15.98 years,9 women and 18 men),and 31 age-and gender-matched healthy controls(aged 49.19±17.51 years,9 women and 22 men)were included in this *** COVID-19 patients with sleep disturbances were included in a longitudinal *** found that COVID-19 patients with sleep disturbances exhibited brain structural changes in almost all brain *** cortical thicknesses of the left pars opercularis and left precuneus were significantly negatively correlated with Pittsburgh Sleep Quality Index ***,we observed changes in the volume of the hippocampus and its subfield regions in COVID-19 patients compared with the healthy *** 3-month follow-up data revealed indices of altered cerebral structure(cortical thickness,cortical grey matter volume,and cortical surface area)in the frontal-parietal cortex compared with the baseline in COVID-19 patients with sleep *** findings indicate that the sleep disturbances patients had altered morphology in the cortical an

关键词： brain structure cortical gray matter volume cortical surface area cortical thickness hippocampus magnetic resonance imaging Pittsburgh Sleep Quality Index severe acute respiratory syndrome coronavirus 2 infections sleep disturbances sub-cortical volume

载体辅助免疫刺激剂通过下调PD-L1和抑制ATP水解增强光动力免疫治疗（英文）

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Science China Materials 2025年

作者：岑怡陈颖蔡华李欣璇陈霞云刘倩倩俞白雪刘已斌王涛李仕颖 The Fifth Affiliated Hospital Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology the NMPA and State Key Laboratory of Respiratory Disease the School of Pharmaceutical Sciences Guangzhou Medical University Graduate School Guangzhou University of Chinese Medicine department of Pulmonary and Critical Care medicine Zhujiang Hospital Southern Medical University

肿瘤细胞存在免疫逃避和免疫抑制特性,极大削弱了免疫激活效应和抗肿瘤免疫疗效.本文开发了一种载体辅助免疫刺激剂(称为CoCeC),通过下调肿瘤细胞程序性死亡配体1 (PD-L1)和抑制三磷酸腺苷(ATP)水解,实现肿瘤光动力免疫治疗.其中,交联...

肿瘤细胞存在免疫逃避和免疫抑制特性,极大削弱了免疫激活效应和抗肿瘤免疫疗效.本文开发了一种载体辅助免疫刺激剂(称为CoCeC),通过下调肿瘤细胞程序性死亡配体1 (PD-L1)和抑制三磷酸腺苷(ATP)水解,实现肿瘤光动力免疫治疗.其中,交联的寡聚壳聚糖是递送二氢卟吩e6和色瑞替尼的药物载体,也是下调PD-L1的免疫佐剂,可抑制肿瘤细胞的免疫逃逸.同时, CoCeC的光动力疗法(PDT)能破坏肿瘤细胞,进而诱导肿瘤细胞发生免疫原性死亡(ICD)并释放损伤相关分子模式(DAMPs),阻断CD39抑制ATP水解为腺苷,从而抑制腺苷造成的肿瘤免疫抑制特性.体外和体内研究结果表明, CoCeC能有效抑制原发性肿瘤的生长,并通过改善肿瘤免疫原性、阻断肿瘤免疫逃逸和逆转肿瘤免疫抑制特性,实现光动力免疫激活和肺转移瘤免疫治疗的目的.这种载体自佐剂策略为纳米药物理性设计提供了新方法,并为逆转多重肿瘤免疫抑制特性和激活抗肿瘤免疫治疗提供了新思路.

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