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Knockdown of RFC4 inhibits the cell proliferation of nasopharyngeal carcinoma and

《医学前沿（英文）》 2023年 第17卷 第1期   页码 132-142 doi: 10.1007/s11684-022-0938-x

摘要： Nasopharyngeal carcinoma (NPC) is a malignant tumor that mainly occurs in East and Southeast Asia. Although patients benefit from the main NPC treatments (e.g., radiotherapy and concurrent chemotherapy), persistent and recurrent diseases still occur in some NPC patients. Therefore, investigating the pathogenesis of NPC is of great clinical significance. In the present study, replication factor c subunit 4 (RFC4) is a key potential target involved in NPC progression via bioinformatics analysis. Furthermore, the expression and mechanism of RFC4 in NPC were investigated in vitro and in vivo. Our results revealed that RFC4 was more elevated in NPC tumor tissues than in normal tissues. RFC4 knockdown induced G2/M cell cycle arrest and inhibited NPC cell proliferation in vitro and in vivo. Interestingly, HOXA10 was confirmed as a downstream target of RFC4, and the overexpression of HOXA10 attenuated the silencing of RFC4-induced cell proliferation, colony formation inhibition, and cell cycle arrest. For the first time, this study reveals that RFC4 is required for NPC cell proliferation and may play a pivotal role in NPC tumorigenesis.

关键词： nasopharyngeal carcinoma     WGCNA     RFC4     proliferation    

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is overexpressed and a prognostic indicator in human breast cancer and promotes breast cancer cell proliferation

null

《医学前沿（英文）》 2016年 第10卷 第1期   页码 41-51 doi: 10.1007/s11684-016-0429-z

摘要：

Midline2 (MID2) is an ubiquitin-conjugating E2 enzyme linked to tumor progression and a novel interacting partner of breast cancer 1, early-onset (BRCA1). However, the role of MID2 in breast cancer remains unknown. This study investigated the expression, prognostic value, and role of MID2 in breast cancer. The expression of MID2 mRNA and protein was significantly upregulated in breast cancer tissue and established cell lines compared with that in normal breast epithelial cells and paired adjacent non-tumor tissue (P<0.001). Immunohistochemical analysis demonstrated that MID2 was overexpressed in 272 of 284 (95.8%) paraffin-embedded, archived breast cancer tissue. Moreover, MID2 expression increased with advanced clinical stage (P<0.001). High MID2 expression was significantly associated with advanced clinical stages and T, N, and M staging (all P<0.05). Univariate and multivariate analyses indicated that high MID2 expression was an independent prognostic factor for poor overall survival in the entire cohort (93.73 vs. 172.1 months; P<0.001, log-rank test) and in subgroups with stages Tis+ I+ II and III+ IV. Furthermore, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide colony formation, and anchorage-independent growth ability assays were conducted. Results showed that siRNA silencing of MID2 expression significantly reduced MCF-7 and MDA-MB-231 cell proliferation in vitro and blocked the growth of MDA-MB-231 cell xenograft tumors in vivo (P<0.05). This study indicated that MID2 may be a novel prognostic marker and interventional target in breast cancer.

关键词： breast cancer     MID2     proliferation     overall survival     xenograft    

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The MYC transcription factor network: balancing metabolism, proliferation and oncogenesis

null

《医学前沿（英文）》 2018年 第12卷 第4期   页码 412-425 doi: 10.1007/s11684-018-0650-z

摘要：

Transcription factor networks have evolved in order to control, coordinate, and separate, the functions of distinct network modules spatially and temporally. In this review we focus on the MYC network (also known as the MAX-MLX Network), a highly conserved super-family of related basic-helix-loop-helix-zipper (bHLHZ) proteins that functions to integrate extracellular and intracellular signals and modulate global gene expression. Importantly the MYC network has been shown to be deeply involved in a broad spectrum of human and other animal cancers. Here we summarize molecular and biological properties of the network modules with emphasis on functional interactions among network members. We suggest that these network interactions serve to modulate growth and metabolism at the transcriptional level in order to balance nutrient demand with supply, to maintain growth homeostasis, and to influence cell fate. Moreover, oncogenic activation of MYC and/or loss of a MYC antagonist, results in an imbalance in the activity of the network as a whole, leading to tumor initiation, progression and maintenance.

关键词： network     transcription     cancer     MYC     MAX     MLX    

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Applications of thermostatically controlled loads for demand response with the proliferation of variable

Meng SONG, Wei SUN

《能源前沿（英文）》 2022年 第16卷 第1期   页码 64-73 doi: 10.1007/s11708-021-0732-5

摘要： More flexibility is desirable with the proliferation of variable renewable resources for balancing supply and demand in power systems. Thermostatically controlled loads (TCLs) attract tremendous attentions because of their specific thermal inertia capability in demand response (DR) programs. To effectively manage numerous and distributed TCLs, intermediate coordinators, e.g., aggregators, as a bridge between end users and dispatch operators are required to model and control TCLs for serving the grid. Specifically, intermediate coordinators get the access to fundamental models and response modes of TCLs, make control strategies, and distribute control signals to TCLs according the requirements of dispatch operators. On the other hand, intermediate coordinators also provide dispatch models that characterize the external characteristics of TCLs to dispatch operators for scheduling different resources. In this paper, the bottom-up key technologies of TCLs in DR programs based on the current research have been reviewed and compared, including fundamental models, response modes, control strategies, dispatch models and dispatch strategies of TCLs, as well as challenges and opportunities in future work.

关键词： thermostatically controlled load     demand response     renewable energy     power system operation    

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is overexpressed and a prognostic indicator in human breast cancer and promotes breast cancer cell proliferation

《医学前沿（英文）》 2021年 第15卷 第6期   页码 942-942 doi: 10.1007/s11684-021-0876-z

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MicroRNA-148b promotes proliferation of hair follicle cells by targeting

Wanbao YANG,Qinqun LI,Bo SU,Mei YU

《农业科学与工程前沿（英文）》 2016年 第3卷 第1期   页码 72-80 doi: 10.15302/J-FASE-2016089

摘要： MicroRNAs (miRNAs), small non-coding RNAs, are involved in many aspects of biological processes. Previous studies have indicated that miRNAs are important for hair follicle development and growth. In our study, we found by qRT-PCR that miR-148b was significantly upregulated in sheep wool follicle bulbs in anagen phase compared with the telogen phase of the hair follicle cycle. Overexpression of miR-148b promoted proliferation of both HHDPC and HHGMC. By using the TOPFlash system we demonstrated that miR-148b could activate Wnt/β-catenin pathway and , , and were consistently upregulated accordingly. Furthermore, transcript factor nuclear factor of activated T cells type 5 ( ) and were predicted to be the target of miR-148b and this was substantiated using a Dual-Luciferase reporter system. Subsequently was further identified as the target of miR-148b using western blotting. These results were considered to indicate that miR-148b could activate the Wnt/β-catenin signal pathway by targeting to promote the proliferation of human hair follicle cells.

关键词： miR-148b     hair follicle     proliferation     NFAT5     Wnt10b    

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Sub-cytotoxic concentrations of ionic silver promote the proliferation of human keratinocytes by inducing

null

《医学前沿（英文）》 2018年 第12卷 第3期   页码 289-300 doi: 10.1007/s11684-017-0550-7

摘要：

Silver-containing preparations are widely used in the management of skin wounds, but the effects of silver ions on skin wound healing remain poorly understood. This study investigated the effects of silver ions (Ag+) on the proliferation of human skin keratinocytes (HaCaT) and the production of intracellular reactive oxygen species (ROS). After treating HaCaT cells with Ag+and/or the active oxygen scavenger N-acetyl cysteine (NAC), cell proliferation and intracellular ROS generation were assessed using CCK-8 reagent and DCFH-DA fluorescent probe, respectively. In addition, 5-bromo-2-deoxyUridine (BrdU) incorporation assays, cell cycle flow cytometry, and proliferating cell nuclear antigen (PCNA) immunocytochemistry were conducted to further evaluate the effects of sub-cytotoxic Ag+ concentrations on HaCaT cells. The proliferation of HaCaT cells was promoted in the presence of 10−6 and 10−5 mol/L Ag+ at 24, 48, and 72 h. Intracellular ROS generation also significantly increased for 5–60 min after exposure to Ag+. The number of BrdU-positive cells and the presence of PCNA in HaCaT cells increased 48 h after the addition of 10−6 and 10−5 mol/L Ag+, with 10−5 mol/L Ag+ markedly increasing the cell proliferation index. These effects of sub-cytotoxic Ag+ concentrations were repressed by 5 mmol/L NAC. Our results suggest that sub-cytotoxic Ag+ concentrations promote the proliferation of human keratinocytes and might be associated with a moderate increase in intracellular ROS levels. This study provides important experimental evidence for developing novel silver-based wound agents or dressings with few or no cytotoxicity.

关键词： ionic silver     human keratinocyte     cell proliferation     reactive oxygen species     active oxygen scavenger     NAC    

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Effect of repeated gonadotropin stimulation on ovarian reserves and proliferation of ovarian surface

Linlin LIANG, Bei XU, Guijin ZHU

《医学前沿（英文）》 2009年 第3卷 第2期   页码 220-226 doi: 10.1007/s11684-009-0037-2

摘要： This study aimed to evaluate the effect of repeated ovarian stimulation (OS) on the ovarian follicular population and morphology in female mice and its influence on the embryo’s developmental ability, and the profile of the ovarian surface epithelium (OSE). A total of 75 mice were enrolled in this experiment and randomly assigned into three groups: repeated ovarian stimulated group [ =25; receiving 5 IU pregnant mare serum gonadotrophin (PMSG) and human chorionic gonadotropin (hCG) at 6 day intervals for 5 cycles]; single ovarian stimulated group ( =25; receiving 5 IU PMSG and hCG for 1 cycle), and control group ( =25; without additional treatment). The follicle number at various stages and the morphologies were recorded respectively in the three groups. The harvested oocytes or embryos, cleavage rate, good quality embryo rate, and blastocyst production rate were counted and calculated, and the proliferations of ovarian surface epithelium were evaluated respectively. In the three groups, the single ovarian stimulation treatment significantly increased the mean number of ovarian oocytes or embryos (39.25±10.77 one-cell embryos/female); on the other hand, repeated gonadotropin stimulation obtained the lowest mean number (5.15± 2.81 eggs/female, <0.01). Repeated ovarian stimulation also tended to decrease normal follicles of primary follicles (66.67%) and secondary follicles (72.86%), and got the lowest cleavage rate (67.47%), lowest good quality embryo rate (2.41%), and lowest blastocyst production rate (0). The OSE cells adjacent to the antral follicles and corpus luteum (CL) in the repeated ovarian stimulated group (81.8%) had a significantly higher proliferation rate than the other groups. The proliferation rate of the OSE in the single ovarian stimulated group (56.4%) was significantly higher than that in the control group (37.5%) ( <0.01). In conclusion, single ovarian stimulation may produce more oocytes/embryos. However, repeated gonadotropin stimulation may have a negative effect on the ovarian follicular quality, the number of mature retrieved oocytes, and the embryo quality, even increasing the chance of ovarian cancer.

关键词： gonadotropin-releasing hormone     ovarian reserve     embryo developmental ability     ovarian surface epithelium    

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Effect of arsenic trioxide on proliferation and apoptosis of U266 cells and its relationship with the

ZHAN Rong, YU Qinghong, HUANG Haobo

《医学前沿（英文）》 2008年 第2卷 第4期   页码 356-360 doi: 10.1007/s11684-008-0068-0

摘要： The aim of this article is to explore the effect of arsenic trioxide (AsO) on the proliferation and apoptosis of myeloma cell line U266 and its relationship with the expression variation of vascular endothelial growth factor (VEGF). The viability and apoptosis of U266 cells were observed by methylthiazolyl- tetrazolium (MTT) assay and terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL). The effect of AsO on the VEGF expression of U266 cells were tested by enzyme linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR) analysis. We found that AsO could significantly inhibit the growth of U266 cells, and the concentration for 50% growth inhibition (IC) was 2 ?mol/L. After treatment with 2, 5, 10 ?mol/L AsO for 36 hours, dose-dependent apoptosis of U266 cells was observed. After treatment with 2, 5, 10 ?mol/L AsO for 72 hours, a dose-dependent reduction of VEGF in the supernatant of U266 cells culture was found. As far as single cells are concerned, nevertheless, the expression of VEGF mRNA did not vary. So we draw the conclusion that AsO could induce the apoptosis of U266 cells and inhibit their proliferation, decrease the tumor load, and lead to the reduction of VEGF in the culture supernatant, but not change the expression of VEGF in single U266 cells.

关键词： VEGF expression     expression variation     culture supernatant     labeling     concentration    

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Zfyve16 regulates the proliferation of B-lymphoid cells

Xuemei Zhao, Donghe Li, Qingsong Qiu, Bo Jiao, Ruihong Zhang, Ping Liu, Ruibao Ren

《医学前沿（英文）》 2018年 第12卷 第5期   页码 559-565 doi: 10.1007/s11684-017-0562-3

摘要：

Zfyve16 (a.k.a. endofin or endosome-associated FYVE-domain protein), a member of the FYVE-domain protein family, is involved in endosomal trafficking and in TGF-β, BMP, and EGFR signaling. The FYVE protein SARA regulates the TGF-β signaling pathway by recruiting Smad2/3 and accelerating their phosphorylation, thereby altering their susceptibility to TGF-β-mediated T cell suppression. Zfyve16 binds to Smad4 and their binding affects the formation of Smad2/3-Smad4 complex in TGF-β signaling. However, the in vivo function of Zfyve16 remains unknown. In this study, we generated a Zfyve16 knockout mouse strain (Zfyve16KO) and examined its hematopoietic phenotypes and hematopoietic reconstruction ability. The proportion of T cells in the peripheral blood of Zfyve16KO mice increases compared with that in wild-type mice. This finding is consistent with the role of Zfyve16 in facilitating TGF-β signaling. Unpredictably, B cell proliferation is inhibited in Zfyve16KO mice. The proliferation potential of Zfyve16KO B-lymphoid cells also significantly decreases in vitro. These results suggest that Zfyve16 inhibits the proliferation of T cells, possibly through the TGF-β signaling, but upregulates the proliferation of B-lymphoid cells.

关键词： Zfyve16     endofin     hematopoiesis     TGF-β     lymphocytes    

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Palmitoylation of GNAQ/11 is critical for tumor cell proliferation and survival in GNAQ/11-mutant uveal

《医学前沿（英文）》 2022年 第16卷 第5期   页码 784-798 doi: 10.1007/s11684-021-0911-0

摘要： More than 85% of patients with uveal melanoma (UM) carry a GNAQ or GNA11 mutation at a hotspot codon (Q209) that encodes G protein α subunit q/11 polypeptides (Gαq/11). GNAQ/11 relies on palmitoylation for membrane association and signal transduction. Despite the palmitoylation of GNAQ/11 was discovered long before, its implication in UM remains unclear. Here, results of palmitoylation-targeted mutagenesis and chemical interference approaches revealed that the loss of GNAQ/11 palmitoylation substantially affected tumor cell proliferation and survival in UM cells. Palmitoylation inhibition through the mutation of palmitoylation sites suppressed GNAQ/11Q209L-induced malignant transformation in NIH3T3 cells. Importantly, the palmitoylation-deficient oncogenic GNAQ/11 failed to rescue the cell death initiated by the knock down of endogenous GNAQ/11 oncogenes in UM cells, which are much more dependent on Gαq/11 signaling for cell survival and proliferation than other melanoma cells without GNAQ/11 mutations. Furthermore, the palmitoylation inhibitor, 2-bromopalmitate, also specifically disrupted Gαq/11 downstream signaling by interfering with the MAPK pathway and BCL2 survival pathway in GNAQ/11-mutant UM cells and showed a notable synergistic effect when applied in combination with the BCL2 inhibitor, ABT-199, in vitro. The findings validate that GNAQ/11 palmitoylation plays a critical role in UM and may serve as a promising therapeutic target for GNAQ/11-driven UM.

关键词： uveal melanoma     mutant GNAQ/11     palmitoylation     BCL2     combination target therapy    

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Effect on proliferation and apoptosis of T24 cell lines via silencing DNMT1 with RNA interference

ZHANG Shilong, ZENG Fuqing, PENG Shibo, WANG Liang

《医学前沿（英文）》 2008年 第2卷 第4期   页码 374-379 doi: 10.1007/s11684-008-0072-4

摘要： Expression of DNA methyltransferase 1 (DNMT1), which plays an important role on aberrantly methylated CpG in the promoter regions of tumor suppressor genes (TSGs), is higher in bladder cancer cells than in normal bladder cells. Therefore, its overexpression is closely related to tumor formation. In this study, the eukaryotic vector pshRNA-DNMT1 was constructed and transfected into T24 cells. Levels of DNMT1 mRNA and protein were detected by reverse transcription-polymerase chain reaction (RT-PCR) and western blot. Relative to the blank control at the 24th, 48th and 72nd hour after transfection of pshRNA-DNMT1, the inhibitory rates of DNMT1 mRNA levels in T24 cells were 28.44%, 52.48%, 70.91%, respectively. Those of DNMT1 proteins were 24.27%, 57.79%, and 77.74%, respectively. Proliferation and apoptosis were assayed by MTT and flow cytometry with Annexin-V-FITC/PI staining. The growth inhibition rates of pshRNA-DNMT1 at the 24th, 48th and 72nd hour after transfection of pshRNA-DNMT1 were (4.34 ± 0.76)%, (9.87 ± 1.54)% and (13.78 ± 1.93)%, respectively. There were statistically significant differences between pshRNA-DNMT1 and the control blank at each time points ( < 0.01); 24, 48 and 72 hours after T24 cells were transfected by pshRNA-DNMT1, the apoptosis rates of pshRNA-DNMT1 were (3.87 ± 0.81)%, (8.69 ± 1.23)% and (11.46 ± 1.24)%, respectively ( < 0.01 blank control). Based on this case, our conclusion is that the recombinant plasmid pshRNA-DNMT1 can silence the expression of gene DNMT1 mRNA and protein effectively, and to some extent, it also can inhibit the proliferation of bladder cancer cell and promote the cellular apoptosis.
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Effect of PRAK gene knockout on the proliferation of mouse embryonic fibroblasts

Xiaowei GONG MD, PhD, Xiaoyan MING MD, Xu WANG MM, Daan WANG MD, Peng DENG MM, Yong JIANG MD, PhD, Aihua LIU MD, PhD,

《医学前沿（英文）》 2009年 第3卷 第4期   页码 379-383 doi: 10.1007/s11684-009-0073-y

摘要： p38 regulated/activated protein kinase (PRAK) plays a key role in cell senescence and tumor suppression. The aim of this study was to investigate if PRAK had effect on cell proliferation. The growth of and mouse embryonic fibroblast (MEF) cells was measured by methylthiazoletetrazolium (MTT) colorimetric assay, and the proportion of the cell number in different phases of the cell cycle was analyzed by flow cytometry. The growth curves showed that the growth rate was notably decreased, and cell double time was elongated in cells; moreover, the number of cells was decreased by 44.5% compared with that of cells cultured for 96h, suggesting that G/M transition is inhibited in cells. Meanwhile, G/S transition was also inhibited in cells, observed with flow cytometry analysis. The ratios of G/G, G/M, and S phases of cells were 44.9%, 12.2%, and 42.9%, respectively, while those of cells were 55.3%, 7.3%, and 37.4%, respectively. There were 23.1% increase and 12.7% decrease of the number of cells in G and S phases comparison with that of cells, respectively. Taken together, gene knockout in MEF cells leads to cell cycle arrest and proliferation inhibition.

关键词： p38 regulated/activated protein kinase     gene knockout     cell cycle     cell proliferation    

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Long non-coding RNA SAP30-2:1 is downregulated in congenital heart disease and regulates cell proliferation

Jing Ma, Shiyu Chen, Lili Hao, Wei Sheng, Weicheng Chen, Xiaojing Ma, Bowen Zhang, Duan Ma, Guoying Huang

《医学前沿（英文）》 2021年 第15卷 第1期   页码 91-100 doi: 10.1007/s11684-020-0778-5

摘要： Congenital heart disease (CHD) is the most common birth defect worldwide. Long non-coding RNAs (lncRNAs) have been implicated in many diseases. However, their involvement in CHD is not well understood. This study aimed to investigate the role of dysregulated lncRNAs in CHD. We used Gene Expression Omnibus data mining, bioinformatics analysis, and analysis of clinical tissue samples and observed that the novel lncRNA SAP30-2:1 with unknown function was significantly downregulated in damaged cardiac tissues from patients with CHD. Knockdown of lncRNA SAP30-2:1 inhibited the proliferation of human embryonic kidney and AC16 cells and decreased the expression of heart and neural crest derivatives expressed 2 (HAND2). Moreover, lncRNA SAP30-2:1 was associated with HAND2 by RNA immunoprecipitation. Overall, these results suggest that lncRNA SAP30-2:1 may be involved in heart development through affecting cell proliferation via targeting HAND2 and may thus represent a novel therapeutic target for CHD.

关键词： congenital heart disease     Gene Expression Omnibus     lncRNA SAP30-2:1     cell proliferation     RNA immunoprecipitation     HAND2    

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NES1/KLK10 and hNIS gene therapy enhanced iodine-131 internal radiation in PC3 proliferation

Jiajia Hu, Wenbin Shen, Qian Qu, Xiaochun Fei, Ying Miao, Xinyun Huang, Jiajun Liu, Yingli Wu, Biao Li

《医学前沿（英文）》 2019年 第13卷 第6期   页码 646-657 doi: 10.1007/s11684-018-0643-y

摘要： gene is thought to be a tumor-suppressor gene. Our previous study found that overexpression of gene in PC3 cell line could slow down the tumor proliferation rate, associated with a mild decrease in expression. The decrease could increase the sensitivity of radiotherapy to tumors. Thus, we supposed to have an “enhanced firepower” effect by combining overexpressed gene therapy and I radiation therapy uptake by overexpressed hNIS protein. We found a weak endogenous expression of hNIS protein in PC3 cells and demonstrated that the low expression of hNIS protein in PC3 cells might be the reason for the low iodine uptake. By overexpressing in PC3, the radioactive iodine uptake ability was significantly increased. Results of and tumor proliferation experiments and F-fluorothymidine ( F-FLT) micro-positron emission tomography/computed tomography (micro-PET/CT) imaging showed that the combined gene therapy and I radiation therapy mediated by overexpressed hNIS protein had the best tumor proliferative inhibition effect. Immunohistochemistry showed an obvious decrease of expression and the lowest expression. These data suggest that via inhibition of expression, overexpressed might enhance the effect of radiation therapy of I uptake in overexpressed PC3 cells.

关键词： androgen-independent prostate cancer     normal epithelial cell-specific 1/kallikrein 10     sodium/iodide symporter     radiation therapy     proliferation    

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标题 作者 时间 类型 操作

Knockdown of RFC4 inhibits the cell proliferation of nasopharyngeal carcinoma and

期刊论文

is overexpressed and a prognostic indicator in human breast cancer and promotes breast cancer cell proliferation

null

期刊论文

The MYC transcription factor network: balancing metabolism, proliferation and oncogenesis

null

期刊论文

Applications of thermostatically controlled loads for demand response with the proliferation of variable

Meng SONG, Wei SUN

期刊论文

is overexpressed and a prognostic indicator in human breast cancer and promotes breast cancer cell proliferation

期刊论文

MicroRNA-148b promotes proliferation of hair follicle cells by targeting

Wanbao YANG,Qinqun LI,Bo SU,Mei YU

期刊论文

Sub-cytotoxic concentrations of ionic silver promote the proliferation of human keratinocytes by inducing

null

期刊论文

Effect of repeated gonadotropin stimulation on ovarian reserves and proliferation of ovarian surface

Linlin LIANG, Bei XU, Guijin ZHU

期刊论文

Effect of arsenic trioxide on proliferation and apoptosis of U266 cells and its relationship with the

ZHAN Rong, YU Qinghong, HUANG Haobo

期刊论文

Zfyve16 regulates the proliferation of B-lymphoid cells

Xuemei Zhao, Donghe Li, Qingsong Qiu, Bo Jiao, Ruihong Zhang, Ping Liu, Ruibao Ren

期刊论文

Palmitoylation of GNAQ/11 is critical for tumor cell proliferation and survival in GNAQ/11-mutant uveal

期刊论文

Effect on proliferation and apoptosis of T24 cell lines via silencing DNMT1 with RNA interference

ZHANG Shilong, ZENG Fuqing, PENG Shibo, WANG Liang

期刊论文

Effect of PRAK gene knockout on the proliferation of mouse embryonic fibroblasts

Xiaowei GONG MD, PhD, Xiaoyan MING MD, Xu WANG MM, Daan WANG MD, Peng DENG MM, Yong JIANG MD, PhD, Aihua LIU MD, PhD,

期刊论文

Long non-coding RNA SAP30-2:1 is downregulated in congenital heart disease and regulates cell proliferation

Jing Ma, Shiyu Chen, Lili Hao, Wei Sheng, Weicheng Chen, Xiaojing Ma, Bowen Zhang, Duan Ma, Guoying Huang

期刊论文

NES1/KLK10 and hNIS gene therapy enhanced iodine-131 internal radiation in PC3 proliferation

Jiajia Hu, Wenbin Shen, Qian Qu, Xiaochun Fei, Ying Miao, Xinyun Huang, Jiajun Liu, Yingli Wu, Biao Li

期刊论文