共查询到20条相似文献,搜索用时 31 毫秒
1.
K. Ba Y. Fu X. Wei Y. Yue G. Li Y. Yao J. Chen X. Cai C. Liang Y. Ge Y. Lin 《Cell proliferation》2013,46(3):312-319
Objective
The aim of this study was to investigate effects of low‐intensity pulsed ultrasound (LIPUS) on differentiation of adipose‐derived stem cells (ASCs), in vitro.Materials and methods
Murine ASCs were treated with LIPUS for either three or five days, immediately after adipogenic induction, or delayed for 2 days. Expression of adipogenic genes PPAR‐γ1, and APN, was examined by real‐time PCR. Immunofluorescence (IF) staining was performed to test for PPAR‐γ at the protein level.Results
Our data revealed that specific patterns of LIPUS up‐regulated levels of both PPAR‐γ1 and APN mRNA, and PPAR‐γ protein.Conclusions
In culture medium containing adipogenic reagents, LIPUS enhanced ASC adipogenesis.2.
3.
Fluoxetine induces autophagic cell death via eEF2K‐AMPK‐mTOR‐ULK complex axis in triple negative breast cancer
下载免费PDF全文
![点击此处可从《Cell proliferation》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Dejuan Sun Lingjuan Zhu Yuqian Zhao Yingnan Jiang Lixia Chen Yang Yu Liang Ouyang 《Cell proliferation》2018,51(2)
Objectives
Triple negative breast cancer (TNBC) is a complex and intrinsically aggressive tumour with poor prognosis, and the discovery of targeted small‐molecule drugs for TNBC treatment still remains in its infancy. In this study, we aimed to discover a small‐molecule agent for TNBC treatment and illuminate its potential mechanisms.Materials and methods
Cell viability was detected by using methylthiazoltetrazolium (MTT) assay. Electron microscopy, GFP‐LC3 transfection, monodansylcadaverine staining and apoptosis assay were performed to determine Fluoxetine‐induced autophagy and apoptosis. Western blotting and siRNA transfection were carried out to investigate the mechanisms of Fluoxetine‐induced autophagy. iTRAQ‐based proteomics analysis was used to explore the underlying mechanisms.Results
We have demonstrated that Fluoxetine had remarkable anti‐proliferative activities and induced autophagic cell death in MDA‐MB‐231 and MDA‐MB‐436 cells. The mechanism for Fluoxetine‐induced autophagic cell death was associated with inhibition of eEF2K and activation of AMPK‐mTOR‐ULK complex axis. Further iTRAQ‐based proteomics and network analyses revealed that Fluoxetine‐induced mechanism was involved in BIRC6, BNIP1, SNAP29 and Bif‐1.Conclusions
These results demonstrate that Fluoxetine induces apoptosis and autophagic cell death in TNBC, which will hold a promise for the future TNBC therapy.4.
5.
A. Di Virgilio L. Tucci M. Scaramuzzino R. Terracciano G. Pelaia R. Savino 《Cell proliferation》2013,46(2):172-182
Objectives
In this study, we have evaluated effects of 24‐hour treatments with simvastatin or rosuvastatin on RAS protein, NF‐κB and MMP expression in LC tissues obtained from 12 patients undergoing thoracic surgery.Materials and methods
Normal and lung tumour tissues obtained from each sample were exposed to simvastatin (2.5–30 μm ) or rosuvastatin (1.25–30 μm ) and western blot analysis was then performed.Results
We documented increased expression of proteins, MMP‐2, MMP‐9 and NF‐κB‐p65 in LC tissues, with respect to normal tissues (P < 0.01). In the malignant tissues, simvastatin and rosuvastatin significantly (P < 0.01) and dose‐dependently reduced RAS protein, MMP‐2/9 and NF‐κB‐p65 expression.Conclusions
In conclusion, our results suggest that simvastatin and rosuvastatin could play a role in LC treatment by modulation of RAS protein, MMP‐2/9 and NF‐κB‐p65.6.
2‐(2‐nitrobenzylidene) indolin‐3‐one compound inhibits transmembrane prostate androgen‐induced protein (TMEPAI) expression and cancer cell proliferation
下载免费PDF全文
![点击此处可从《Cell proliferation》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Yuyin Li Jianjun Wang Ning Song Feihong Zeng Miaomiao Zhao Ali Wang Yue Chen Lei Jing Peng Yu Aipo Diao 《Cell proliferation》2018,51(5)
Objectives
The transmembrane prostate androgen‐induced protein (TMEPAI) is aberrantly expressed in many cancer and plays a crucial role in tumourigenesis, which makes it a potential cancer therapeutic target for drug discovery.Materials and methods
Here, we employed a firefly luciferase reporter driven by the TMEPAI gene promoter to screen for compound capable of inhibiting the expression of TMEPAI, and the effects of TMEPAI inhibitor on cancer cell proliferation were evaluated using the colony formation assay, cell cycle analysis, Ki‐67 immunofluorescence assay and EdU incorporation assay.Results
2‐(2‐nitrobenzylidene) indolin‐3‐one (JHY‐A007‐50) was identified and shown to effectively inhibit the TMEPAI promoter activity. Further studies revealed that JHY‐A007‐50 specifically inhibited the expression of TMEPAI at both the mRNA and protein levels. Moreover, we found that JHY‐A007‐50 could inhibit cell proliferation and induce cell cycle arrest at the G1 phase. Our results showed that overexpression of TMEPAI decreased the inhibitory effects of JHY‐A007‐50 on cancer cell proliferation, and JHY‐A007‐50 did not affect the cell viability of HeLa cells knocked down of TMEPAI.Conclusions
Taken together, these results suggest that compound JHY‐A007‐50 mediates the downregulation of TMEPAI expression and inhibits cell proliferation in cancer cells.7.
Critical role of inflammatory mast cell in fibrosis: Potential therapeutic effect of IL‐37
下载免费PDF全文
![点击此处可从《Cell proliferation》网站下载免费的PDF全文](/ch/ext_images/free.gif)
P. Conti Al. Caraffa F. Mastrangelo L. Tettamanti G. Ronconi I. Frydas S. K. Kritas T. C. Theoharides 《Cell proliferation》2018,51(5)
Background
Fibrosis involves the activation of inflammatory cells, leading to a decrease in physiological function of the affected organ or tissue.Aims
To update and synthesize relevant information concerning fibrosis into a new hypothesis to explain the pathogenesis of fibrosis and propose potential novel therapeutic approaches.Materials and Methods
Literature was reviewed and relevant information is discussed in the context of the pathogenesis of fibrosis.Results
A number of cytokines and their mRNA are involved in the circulatory system and in organs of patients with fibrotic tissues. The profibrotic cytokines are generated by several activated immune cells, including fibroblasts and mast cells (MCs), which are important for tissue inflammatory responses to different types of injury. MC‐derived TNF, IL‐1, and IL‐33 contribute crucially to the initiation of a cascade of the host defence mechanism(s), leading to the fibrosis process. Inhibition of TNF and inflammatory cytokines may slow the progression of fibrosis and improve the pathological status of the affected subject. IL‐37 is generated by various types of immune cells and is an IL‐1 family member protein. IL‐37 is not a receptor antagonist; it binds IL‐18 receptor alpha (IL‐18Rα) and delivers the inhibitory signal by using TIR8. It has been shown that IL‐37 can be protective in inflammation and injury, and inhibits both innate and adaptive immunity.Discussion
IL‐37 may be useful for suppression of inflammatory diseases induced by inhibiting MyD88‐dependent TLR signalling. In addition, IL‐37 downregulates NF‐κB induced by TLR2 or TLR4 through a mechanism dependent on IL‐18Rα.Conclusion
This review summarizes current knowledge on the role of MC in inflammation and tissue/organ fibrosis, with a focus on the therapeutic potential of IL‐37‐targeting cytokines.8.
FBXW7 suppresses epithelial‐mesenchymal transition and chemo‐resistance of non‐small‐cell lung cancer cells by targeting snai1 for ubiquitin‐dependent degradation
下载免费PDF全文
![点击此处可从《Cell proliferation》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Guodong Xiao Yuan Li Meng Wang Xiang Li Sida Qin Xin Sun Rui Liang Boxiang Zhang Ning Du Chongwen Xu Hong Ren Dapeng Liu 《Cell proliferation》2018,51(5)
Objectives
FBXW7 acts as a tumour suppressor by targeting at various oncoproteins for ubiquitin‐mediated degradation. However, the clinical significance and the involving regulatory mechanisms of FBXW7 manipulation of NSCLC regeneration and therapy response are not clear.Materials and Methods
Immunohistochemical staining and qRT‐PCR were applied to detect FBXW7 and Snai1 expression in 100 samples of NSCLC and matched tumour‐adjacent tissues. FBXW7 manipulation of cancer biological functions were studied by using MTT assay, immunoblotting, flow cytometry, transwells, wound healing assay, and sphere‐formation assays. Immunofluorescence and co‐immunoprecipitation were used to analyse the possible interaction between Snai1 and FBXW7.Results
We detected the decreased FBXW7 expression in majority of the NSCLC tissues, and lower FBXW7 level was correlated with advanced TNM stage. Furthermore, those patients with decreased FBXW7 expression tend to have both poorer 5‐year survival outcomes, and shorter disease‐free survival, comparing to those with higher FBXW7 levels. Functionally, we found that FBXW7 enforcement suppressed NSCLC progression by inducing cell growth arrest, increasing chemo‐sensitivity and inhibiting Epithelial‐mesenchymal Transition (EMT) progress. Results further showed that FBXW7 could interact with Snai1 directly to degrade its expression through ubiquitylating alternation in NSCLC, which could be partially abrogated by restoring Snai1 expression.Conclusions
FBXW7 conduction of tumour suppression was partly through degrading Snai1 directly for ubiquitylating regulation in NSCLC9.
Schisandrin B down‐regulated lncRNA BCYRN1 expression of airway smooth muscle cells by improving miR‐150 expression to inhibit the proliferation and migration of ASMC in asthmatic rats
下载免费PDF全文
![点击此处可从《Cell proliferation》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Xiao‐yu Zhang Xue‐yi Tang Li‐jun Ma Ya‐li Guo Xiao‐su Li Li‐min Zhao Cui‐jie Tian Dong‐Jun Cheng Zhuo‐chang Chen Luo‐xian Zhang 《Cell proliferation》2017,50(6)
Objective
The mechanism of Schisandrin B on the proliferation and migration of airway smooth muscle cells (ASMCs) in asthmatic rats was explored.Methods
SD rats were divided into three groups: control (group 1), model (group 2) and model + Schisandrin B (group 3). miR‐150 and lncRNA BCYRN1 levels were measured by qRT‐PCR. The combination of BCYRN1 and miR‐150 was detected by RNA pull down. ASMCs’ viability/proliferation/migration were examined by WST‐1 assay and 24‐well Transwell system.Results
Schisandrin B up‐regulated miR‐150 expression and down‐regulated BCYRN1 expression in sensitized rats. Schisandrin B reversed the expression of miR‐150 and BCYRN1 in MV‐treated ASMCs. In addition, Schisandrin B inhibited the viability, proliferation and migration of MV‐induced ASMCs. We also found miR‐150 inhibited BCYRN1 expression which was proved by experiments using ASMCs transfected with miR‐150 inhibitor.Conclusion
Schisandrin B increased miR‐150 expression and decreased BCYRN1, and BCYRN1 expression was inhibited by miR‐150, which indicated that Schisandrin B could regulate BCYRN1 through miR‐150.10.
Objectives
Donor specific antibodies (DSA) and a positive cross‐match are contraindications for kidney transplantation. Trials of allograft transplantation across the HLA barrier have employed desensitization strategies, including the use of plasmapheresis, intravenous immunoglobulins, anti‐B‐cell monoclonal antibodies and splenectomy, associated with high‐intensity immunosuppressive regimens. Our case 1 report suffered from repeatedly positive lymphocyte cross match after 1st renal transplantation. Graft nephrectomy could not correct the state of sensitization. Splenectomy was done in a trial to get rid of the antibody producing clone. Furthermore plasmapheresis with low dose IVIG could not as well revert the state of sensitization for the patient.Material and methods
About 50 millions donor specific MSCs were injected to the patient.Results
MSCs transfusion proved to be the only procedure which could achieve successful desensitization before performing the second transplantation owing to their immunosuppressive properties.Conclusion
This case indicates that DS‐MSCs is a potential option for anti‐HLA desensitization. In cases 2 and 3 IV DS‐MSCs transfusion was selected from the start as a successful line of treatment for pre renal transplantation desensitization to save other unnecessary lines of treatment that were tried in case 1.11.
Loss‐of‐function of miR‐142 by hypermethylation promotes TGF‐β‐mediated tumour growth and metastasis in hepatocellular carcinoma
下载免费PDF全文
![点击此处可从《Cell proliferation》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Qiangfeng Yu Leyang Xiang Libo Yin Xincheng Liu Dinghua Yang Jianyin Zhou 《Cell proliferation》2017,50(6)
Objectives
Hypermethylation‐induced epigenetic silencing of tumour suppressor genes (TSGs) are frequent events during carcinogenesis. MicroRNA‐142 (miR‐142) is found to be dysregulated in cancer patients to participate into tumour growth, metastasis and angiogenesis. However, the tumour suppressive role of miR‐142 and the status of methylation are not fully understood in hepatocellular carcinoma (HCC).Methods
Hepatocellular carcinoma tissues and corresponding non‐neoplastic tissues were collected. The expression and function of miR‐142 and TGF‐β in two HCC cell lines were determined. The miRNA‐mRNA network of miR‐142 was analysed in HCC cell lines.Results
We found that the miR‐142 expression was reduced in tumour tissues and two HCC cell lines HepG2 and SMMC7721, which correlated to higher TNM stage, metastasis and differentiation. Moreover, miR‐142 was identified to directly target and inhibit transforming growth factor β (TGF‐β), leading to decreased cell vitality, proliferation, EMT and the ability of pro‐angiogenesis in TGF‐β‐dependent manner. Interestingly, the status of methylation of miR‐142 was analysed and the results found the hypermethylated miR‐142 in tumour patients and cell lines. The treatment of methylation inhibitor 5‐Aza could restore the expression of miR‐142 to suppress the TGF‐β expression, which impaired TGF‐β‐induced tumour growth.Conclusion
These findings implicated that miR‐142 was a tumour suppressor gene in HCC and often hyermethylated to increase TGF‐β‐induced development of hepatocellular carcinoma.12.
13.
14.
S.‐H. Kim S. H. Bang S. A. Park S. Y. Kang K. D. Park I. U. Oh S. H. Yoo H. Kim C.‐H. Kim S. Y. Baek 《Cell proliferation》2013,46(3):291-299
Objectives
While most human adipose tissues, such as those located in the abdomen, hip and thigh, are of mesodermal origin, adipose tissues located in the face are of ectodermal origin. The present study has compared stem cell‐related features of abdomen‐derived adult stem cells (A‐ASCs) with those of eyelid‐derived adult stem cells (E‐ASCs).Materials and methods
Adipose tissue‐derived cells were maintained in DMEM supplemented with 10% FBS. Before passage 6, cells were analysed using FACS, immunocytochemistry and quantitative real time PCR (qRT‐PCR). To examine multi‐differentiational potential, early passage ASCs were cultivated in each of a commercial Stempro® Differentiation kit.Results
Unlike fibroblast‐like morphology of A‐ASCs, E‐ASCs had bipolar morphology. Both types of cell exhibited similar surface antigens, and neuronal cell‐related genes and proteins. However, there were differences in mRNA expression levels of CD90 and CD146; neuron‐specific enolase (NSE) and nuclear receptor‐related protein 1 (Nurr1) were different between the two cell types. There was no difference in multi‐differentiational potential between 3 E‐ASCs lines, however, E‐ASCs had higher expression levels of chondrocyte‐related genes compared to A‐ASCs. These cells underwent senescence and maintained normal karyotypes.Conclusions
Although isolated from similar adipose tissues, both types of cells displayed many contrasting characteristics. Understanding defining phenotypes of such cells is useful for making suitable choices in differing clinical indications.15.
Galantamine inhibits β‐amyloid‐induced cytostatic autophagy in PC12 cells through decreasing ROS production
下载免费PDF全文
![点击此处可从《Cell proliferation》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Sheng Jiang Ye Zhao Tao Zhang Jingbin Lan Jing Yang Longhui Yuan Qiyu Zhang Kejian Pan Kun Zhang 《Cell proliferation》2018,51(3)
Objectives
Alzheimer's disease (AD) is one of the most prevalent brain diseases among the elderly, majority of which is caused by abnormal deposition of amyloid beta‐peptide (Aβ). Galantamine, currently the first‐line drug in treatment of AD, has been shown to diminish Aβ‐induced neurotoxicity and exert favourable neuroprotective effects, but the detail mechanisms remain unclear.Materials and methods
Effects of galantamine on Aβ‐induced cytotoxicity were checked by MTT, clone formation and apoptosis assays. The protein variations and reactive oxygen species (ROS) production were measured by western blotting analysis and dichloro‐dihydro‐fluorescein diacetate assay, respectively.Results
Galantamine reversed Aβ‐induced cell growth inhibition and apoptosis in neuron cells PC12. Aβ activated the entire autophagy flux and accumulation of autophagosomes, and the inhibition of autophagy decreased the protein level of cleaved‐caspase‐3 and Aβ‐induced cytotoxicity. Meanwhile, galantamine suppressed Aβ‐mediated autophagy flux and accumulation of autophagosomes. Moreover, Aβ upregulated ROS accumulation, while ROS scavengers N‐acetyl‐l ‐cysteine impaired Aβ‐mediated autophagy. Further investigation showed that galantamine downregulated NOX4 expression to inhibit Aβ‐mediated ROS accumulation and autophagy.Conclusions
Galantamine inhibits Aβ‐induced cytostatic autophagy through decreasing ROS accumulation, providing new insights into deep understanding of AD progression and molecular basis of galantamine in neuroprotection.16.
A novel inhibitor of ADAM17 sensitizes colorectal cancer cells to 5‐Fluorouracil by reversing Notch and epithelial‐mesenchymal transition in vitro and in vivo
下载免费PDF全文
![点击此处可从《Cell proliferation》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Dan‐Dan Li Chang‐Hao Zhao Huai‐Wei Ding Qiong Wu Tian‐Shu Ren Jian Wang Cong‐Qin Chen Qing‐Chun Zhao 《Cell proliferation》2018,51(5)
Objectives
Colorectal cancer is one of the most common malignancies both in men and women. Owing to metastasis and resistance, the prognosis of colorectal cancerCRC patients remains extremely poor with chemotherapy. A disintegrin and metalloproteinase 17 (ADAM17) induces the activation of Notch pathway and contributes to the chemoresistance. This study aimed to discover a novel ADAM17 inhibitor and investigate the chemosensitization effect.Materials and methods
Pharmacophore model, western blot and enzymatic assay were used to discover ZLDI‐8. Cell proliferation was determined by MTT and colony formation assay. Cell migratory and invasive ability were determined by wound healing scratch and transwell assay. Immunofluorescence images and western blot analysed the expression of Notch or epithelial‐mesenchymal transition (EMT) pathway markers. Xenografts were employed to evaluate the chemosensitization effect of ZLDI‐8 in vivo.Results
We found that ZLDI‐8 cell‐specifically inhibited the proliferation of CRC, and this effect was due to abrogation of ADAM17 and Notch pathway. Meanwhile, we reported for the first time that ZLDI‐8 synergistically improved the anti‐tumour and anti‐metastasis activity of 5‐fluorouracil or irinotecan by reversing Notch and EMT pathways. Interestingly, in vivo studies further demonstrated that ZLDI‐8 promoted the anti‐tumour effect of 5‐fluorouracil through Notch and EMT reversal.Conclusions
A novel ADAM17 inhibitor ZLDI‐8 may be a potential chemosensitizer which sensitized CRC cells to 5‐fluorouracil or irinotecan by reversing Notch and EMT pathways.17.
Objectives
Human CAP10‐like protein 46 kDa (hCLP46), also known as Poglut1, has been shown to be an essential regulator of Notch signalling. hCLP46 is overexpressed in primary acute myelogenous leukaemia, T‐acute lymphoblastic leukaemia samples and other leukaemia cell lines. However, effects of hCLP46 overexpression, up to now, have remained unknown.Materials and methods
In this study, we established stable 293TRex cell lines inducibly overexpressing hCLP46, and knocked down hCLP6 with a specific small interfering RNA to explore function of the protein in Notch signalling and cell proliferation.Results
hCLP46 overexpression enhanced Notch1 activation in 293Trex cells in a ligand‐dependent manner, with increased Notch signalling enhancing Hes1 expression. We further verified that overexpression of hCLP46 inhibited proliferation of 293TRexs and was correlated with increases in cyclin dependent kinase inhibitors p21 and p27, whereas reduced hCLP46 expression moderately increased cell proliferation. In addition, p21 and p27 protein levels were higher when Notch signalling was activated by EDTA treatment.Conclusions
Taken together, hCLP46 enhanced Notch activation and inhibited 293TRex cell proliferation through CDKI signalling.18.
Extremely low‐frequency electromagnetic fields accelerates wound healing modulating MMP‐9 and inflammatory cytokines
下载免费PDF全文
![点击此处可从《Cell proliferation》网站下载免费的PDF全文](/ch/ext_images/free.gif)
A. Patruno A. Ferrone E. Costantini S. Franceschelli M. Pesce L. Speranza P. Amerio C. D'Angelo M. Felaco A. Grilli M. Reale 《Cell proliferation》2018,51(2)
Objectives
In our previous reports, we have demonstrated that extremely low‐frequency electromagnetic fields (ELF‐EMF) exposure enhances the proliferation of keratinocyte. The present study aimed to clarify effects of ELF‐EMF on wound healing and molecular mechanisms involved, using a scratch in vitro model.Materials and methods
The wounded monolayer cultures of human immortalized keratinocytes (HaCaT), at different ELF‐EMF and Sham exposure times were monitored under an inverted microscope. The production and expression of IL‐1β, TNF‐α, IL‐18 and IL‐18BP were measured by enzyme‐linked immunosorbent assay and quantitative real‐time PCR. The activity and the expression of matrix metalloproteinases (MMP)‐2/9 was evaluated by zymography and Western blot analysis, respectively. Signal transduction proteins expression (Akt and ERK) was measured by Western blot.Results
The results of wound healing in vitro assay revealed a significant reduction of cell‐free area time‐dependent in ELF‐EMF‐exposed cells compared to Sham condition. Gene expression and release of cytokines analysed were significantly increased in ELF‐EMF‐exposed cells. Our results further showed that ELF‐EMF exposure induced the activity and expressions of MMP‐9. Molecular data showed that effects of ELF‐EMF might be mediated via Akt and ERK signal pathway, as demonstrated using their specific inhibitors.Conclusions
Our results highlight ability of ELF‐EMF to modulate inflammation mediators and keratinocyte proliferation/migration, playing an important role in wound repair. The ELF‐EMF accelerates wound healing modulating expression of the MMP‐9 via Akt/ERK pathway.19.
Sustained release of stem cell factor in a double network hydrogel for ex vivo culture of cord blood‐derived CD34+ cells
下载免费PDF全文
![点击此处可从《Cell proliferation》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Objectives
Stem cell factor (SCF) is considered as a commonly indispensable cytokine for proliferation of haematopoietic stem cells (HSCs), which is used in large dosages during ex vivo culture. The work presented here aimed to reduce the consumption of SCF by sustained release but still support cells proliferation and maintain the multipotency of HSCs.Materials and methods
Stem cell factor was physically encapsulated within a hyaluronic acid/gelatin double network (HGDN) hydrogel to achieve a slow release rate. CD34+ cells were cultured within the SCF‐loaded HGDN hydrogel for 14 days. The cell number, phenotype and functional capacity were investigated after culture.Results
The HGDN hydrogels had desirable properties and encapsulated SCF kept being released for more than 6 days. SCF remained the native bioactivity, and the proliferation of HSCs within the SCF‐loaded HGDN hydrogel was not affected, although the consumption of SCF was only a quarter in comparison with the conventional culture. Moreover, CD34+ cells harvested from the SCF‐loaded HGDN hydrogels generated more multipotent colony‐forming units (CFU‐GEMM).Conclusion
The data suggested that the SCF‐loaded HGDN hydrogel could support ex vivo culture of HSCs, thus providing a cost‐effective culture protocol for HSCs.20.
SATB2 targeted by methylated miR‐34c‐5p suppresses proliferation and metastasis attenuating the epithelial‐mesenchymal transition in colorectal cancer
下载免费PDF全文
![点击此处可从《Cell proliferation》网站下载免费的PDF全文](/ch/ext_images/free.gif)