scholarly journals MicroRNA-1253 Suppresses Cell Proliferation Migration and Invasion of Osteosarcoma by Targeting MMP9

2021 ◽  
Vol 20 ◽  
pp. 153303382199527
Author(s):  
Jianwen Mo ◽  
Tiansheng Zheng ◽  
Li Lei ◽  
Peng Dai ◽  
Jun Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Real Time ◽  
Real Time Pcr ◽  
Target Genes ◽  
Migration And Invasion ◽  
Quantitative Real Time Pcr ◽  
Osteoblast Cells ◽  
Downstream Target ◽  
Cell Functions

Purpose: MicroRNAs play an important role in osteosarcoma (OS) development and progress. Although miR-1253 was considered as a tumor-inhibitor in some cancers, it’s function in the OS is not clear. Methods: In our study, we examined the expression of miR-1253 in OS cells and osteoblast cells using quantitative real-time PCR. The proliferation of OS cells was measured by BrdU assay, and we performed transwell to detect migration and invasion of OS cells. Meanwhile, EMT proteins were tested by western blot. We used Bioinformatics to predict the target genes of miR-1253 and found out Matrix metalloproteinases9 (MMP9) was one of that. The direct combination between miR-1253 and MMP9 was verified by double luciferase reporting experiment. Quantitative real-time PCR and western blot were used to detect the expression of MMP9. Results: We found that the expression level of miR-1253 in OS cells was significantly lower than that in osteoblast cells. Overexpression of miR-1253 could significantly inhibit OS cell proliferation, migration, invasion and EMT. And then, MMP9 was predicted as a downstream target of miR-1253 by Bioinformatics analysis. Further experiments showed that miR-1253 could reduce the protein level of MMP9 by directly binding to the 3’-UTR of MMP9. Afterward, we performed a rescue experiment, in which both MMP9 and miR-1253 were overexpressed. Compared with the groups overexpressed miR-1253 alone, cell proliferation, migration and invasion in co-overexpression groups were improved. Conclusions: In summary, these results suggested that miR-1253 down-regulated in OS cells, and could suppress the proliferation, migration and invasion of OS cells. Its molecular regulatory mechanism was that inhibits the expression of the downstream target gene MMP9 by directly binding, thus affect OS cell functions. Therefore, miR-1253 has the potential to become a biomarker and therapeutic target for OS therapy.

scholarly journals Έκφραση του σηματοδοτικού μονοπατιού Notch σε πλακούντες εγκύων με προεκλαμψία

2015 ◽  
Author(s):  
Περσεφόνη Φραγκιαδάκη
Keyword(s):  
Western Blot ◽  
Notch Signaling ◽  
Real Time ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Target Genes ◽  
Notch Signaling Pathway ◽  
Quantitative Real Time Pcr ◽  
Notch 1 ◽  
Qrt Pcr

Η προεκλαμψία αποτελεί μια από τις κυριότερες αιτίες μητρικής και εμβρυικής/νεογνικής νοσηρότητας και θνητότητας και επιπλέκει το 3-5% των κυήσεων. Προηγούμενες μελέτες έδειξαν ότι μέλη του σηματοδοτικού μονοπατιού Notch (Notch signaling pathway) εκφράζονται στον πλακούντα και παίζουν σημαντικό ρόλο στην ομαλή ανάπτυξη του ενεργοποιώντας μεταγραφικούς παράγοντες οι οποίοι αλλάζουν την έκφραση γονιδίων στόχων. Διαταραχές στη λειτουργία του μονοπατίου Notch σχετίζονται με παθολογική πλακουντοποίηση. Σκοπός της μελέτης αυτής είναι να εξετάσει την έκφραση των υποδοχέων (receptors) NOTCH1,-2,-3,-4, των συνδετών (ligands) DLL1,-3,-4, JAG1,-2 και των γονιδίων στόχων (target genes) HEY1,-2 σε πλακούντες κυήσεων με προεκλαμψία. Εξετάστηκαν δείγματα πλακουντιακού ιστού από 20 προεκλαμπτικές και από 20 φυσιολογικές κυήσεις. Τα επίπεδα mRNA των υπό εξέταση μορίων μετρήθηκαν με ποσοτική (quantitative) Real-Time PCR (qRT-PCR) ενώ η πρωτεϊνική έκφραση της ενδοκυττάριας περιοχής (intracellular domain) των NOTCH2 (NICD2) και NOTCH3 (NICD3) εκτιμήθηκαν με Western Blot (WB). Τα αποτελέσματα μας έδειξαν ότι οι υποδοχείς Notch-1 και Notch-4 αλλά και ο συνδέτης Dll-1 δεν εκφράζονται στους πλακούντες γυναικών με προεκλαμψία ή με φυσιολογική εγκυμοσύνη. Ωστόσο, τα επίπεδα έκφρασης mRNA των NOTCH2, NOTCH3, DLL3, DLL4, JAG1, JAG2, HEY1 and HEY2 ήταν μειωμένα στα παθολογικά δείγματα σε σχέση με τα φυσιολογικά (p<0.01). Η ανάλυση με WB επιβεβαίωσε ότι τα επίπεδα πρωτεϊνικής έκφρασης των NICD2 και NICD3 ήταν επίσης ελαττωμένα στα δείγματα της προεκλαμψίας (p=0.014 και p<0.001, αντίστοιχα). Περαιτέρω στατιστική ανάλυση έδειξε α) μη έκφραση σε γονιδιακό επίπεδο του υποδοχέα NOTCH3 στις εγκύους εκείνες που κάπνιζαν και στη διάρκεια της εγκυμοσύνης σε σχέση με εκείνες που το έκοψαν (p=0.029) και β) στις περιπτώσεις με προεκλαμψία και βάρος νεογνού μικρότερο από την 5η εκατοστιαία θέση παρατηρήσαμε υψηλότερα επίπεδα πρωτεΐνης του NICD-3 (p=0.028) και υψηλότερα επίπεδα mRNA του Dll-3 (p=0.041). Τα αποτελέσματα της μελέτης μας δείχνουν ότι το σηματοδοτικό μονοπάτι Notch αποτελεί σημαντικό μέρος της παθογένειας αυτής της επιπλοκής της εγκυμοσύνης. Περαιτέρω μελέτες απαιτούνται με σκοπό να διερευνηθεί βαθύτερα και να καθοριστεί ο ρόλος των εξετασθέντων μορίων στην προεκλαμψία και να μελετηθεί η δυνητική τους χρήση στην πρόβλεψη και τη διαγνωστική και θεραπευτική προσέγγιση της νόσου.

scholarly journals KLK11 promotes the activation of mTOR and protein synthesis to facilitate cardiac hypertrophy

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yi Wang ◽  
Hongjuan Liao ◽  
Yueheng Wang ◽  
Jinlin Zhou ◽  
Feng Wang ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Western Blot ◽  
Real Time ◽  
Real Time Pcr ◽  
Mtor Signaling ◽  
Heart Weight ◽  
Cardiomyocyte Hypertrophy ◽  
Quantitative Real Time Pcr

Abstract Background Cardiovascular diseases have become the leading cause of death worldwide, and cardiac hypertrophy is the core mechanism underlying cardiac defect and heart failure. However, the underlying mechanisms of cardiac hypertrophy are not fully understood. Here we investigated the roles of Kallikrein 11 (KLK11) in cardiac hypertrophy. Methods Human and mouse hypertrophic heart tissues were used to determine the expression of KLK11 with quantitative real-time PCR and western blot. Mouse cardiac hypertrophy was induced by transverse aortic constriction (TAC), and cardiomyocyte hypertrophy was induced by angiotensin II. Cardiac function was analyzed by echocardiography. The signaling pathway was analyzed by western blot. Protein synthesis was monitored by the incorporation of [3H]-leucine. Gene expression was analyzed by quantitative real-time PCR. Results The mRNA and protein levels of KLK11 were upregulated in human hypertrophic hearts. We also induced cardiac hypertrophy in mice and observed the upregulation of KLK11 in hypertrophic hearts. Our in vitro experiments demonstrated that KLK11 overexpression promoted whereas KLK11 knockdown repressed cardiomyocytes hypertrophy induced by angiotensin II, as evidenced by cardiomyocyte size and the expression of hypertrophy-related fetal genes. Besides, we knocked down KLK11 expression in mouse hearts with adeno-associated virus 9. Knockdown of KLK11 in mouse hearts inhibited TAC-induced decline in fraction shortening and ejection fraction, reduced the increase in heart weight, cardiomyocyte size, and expression of hypertrophic fetal genes. We also observed that KLK11 promoted protein synthesis, the key feature of cardiomyocyte hypertrophy, by regulating the pivotal machines S6K1 and 4EBP1. Mechanism study demonstrated that KLK11 promoted the activation of AKT-mTOR signaling to promote S6K1 and 4EBP1 pathway and protein synthesis. Repression of mTOR with rapamycin blocked the effects of KLK11 on S6K1 and 4EBP1 as well as protein synthesis. Besides, rapamycin treatment blocked the roles of KLK11 in the regulation of cardiomyocyte hypertrophy. Conclusions Our findings demonstrated that KLK11 promoted cardiomyocyte hypertrophy by activating AKT-mTOR signaling to promote protein synthesis.

CircRNA profiling identifies circRNF180 as a tumor suppressor in hepatocellular carcinoma

Epigenomics ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 513-530
Author(s):  
Xi Zeng ◽  
Chao Tan ◽  
Meile Mo ◽  
Xiaoling Qin ◽  
Xiaoyun Ma ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Suppressor ◽  
Real Time ◽  
Real Time Pcr ◽  
Expression Profiles ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Quantitative Real Time Pcr ◽  
Potential Biomarker ◽  
Hcc Cells

Aim: To explore the expression profiles and functions of circRNAs in hepatocellular carcinoma (HCC). Materials & methods: We obtained circRNA expression profiles through RNA sequencing. Expression levels of circRNAs were confirmed by quantitative real-time PCR. The effects on HCC progression were determined using Cell Counting Kit 8, clone formation and transwell assays. Results: We identified 114 upregulated and 144 downregulated circRNAs in HCC tissues. The results of quantitative real-time PCR showed that circGNAO1, circRNF180 and circMERTK were significantly downregulated in HCC tissues, whereas circSNX6 was significantly upregulated. CircRNF180 was associated with microvascular invasion. Overexpression of circRNF180 inhibits the proliferation, colony formation, migration and invasion of HCC cells. Conclusion: CircRNF180 may function as a tumor suppressor and could serve as a potential biomarker and therapeutic target in HCC.

miR-184 Inhibits Inflammation Through Targeting Toll-Like Receptor 4 (TLR4)/NLR Family Pyrin Domain Containing 3 (NLRP3) Signaling Pathway in Neonatal Purulent Meningitis

2020 ◽  
Vol 10 (4) ◽  
pp. 569-575
Author(s):  
Jiang Wu ◽  
Shixiong Yang ◽  
Jin Shi ◽  
Yibing Shi
Keyword(s):  
Cell Proliferation ◽  
Cerebrospinal Fluid ◽  
Western Blot ◽  
Real Time ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Caspase 3 ◽  
Caspase 1 ◽  
Purulent Meningitis ◽  
Inflammation Group

Neonatal purulent meningitis (NPM) leads to higher mortality and neurological sequelae rates. miR184 involves in inflammation and tumor, but the role of miR-184 in NPM remains unclear. NPM patients and non-intracranial infected neonates were collected and miR-184 expression in cerebrospinal fluid was assessed by real-time PCR. The Neuro-2a cell line was cultured and divided into control group, inflammation group (treated with LPS), and miR-184 inhibitor group, which was transfected with miR-184 inhibitor on the basis of inflammation followed by analysis of miR-184 and TLR4 expression by Real time PCR, Caspase 3 activity, cell proliferation by MTT assay, secretion of IL-1β and IL-6 by ELISA, NLRP3 expression by real time PCR and western blot, and Caspase-1 p20 and NF- B level by western blot. miR-184 expression level was significantly increased in cerebrospinal fluid of NPM group (P < 0 05) and also elevated in inflammation group along with significantly inhibited cell proliferation was inhibited, increased Caspase 3 activity, IL-1β and IL-6 secretion, and decreased TLR4, NLRP3, Caspase-1 p20 and NFκ- B expression (P < 0 05). miR-184 inhibitor significantly down-regulated miR-184 expression in the inflammation group, promoted cell proliferation, decreased Caspase 3 activity, IL-1β and IL-6 secretion, and increased TLR4, NLRP3, Caspase1 p20 and NF- κB expression (P < 0 05). miR-184 expression is increased in neonatal purulent meningitis and it can inhibit inflammation by targeting TLR4/NLRP3 signaling pathway, leading to amelioration of the progression of neonatal purulent meningitis.

miR-184 Inhibits Hypertrophic Scar Through Regulating Phosphatidylinositol 3-Kinase (PI3K)/Protein Kinase B (AKT) Signaling Pathway

2020 ◽  
Vol 10 (1) ◽  
pp. 133-138
Author(s):  
Peng Zhao ◽  
Junxia Qin ◽  
Lili Liang ◽  
Xinzhong Zhang
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Real Time ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Hypertrophic Scar ◽  
Scar Tissue ◽  
Akt Signaling ◽  
Scar Formation ◽  
Akt Signaling Pathway

Hypertrophic scar (HS) is a process of tissue repair and healing, and excessive fibrosis of local tissue leads to scar formation. During HS formation, fibroblasts (Fb) proliferate, synthesize and secrete and promote HS development. miR-184 regulates skin formation and tissue development. However, miR-184’s role in HS remains unclear. miR-184 expression in HS patients and normal healthy (Control) tissues was measured by real-time PCR. pAKT expression was analyzed by Western blot. Fb cells from human HS were cultured and divided into 2 groups, siRNA NC group and miR-184 siRNA group followed by analysis of miR-184 expression by real time PCR, cell proliferation by MTT assay, secretion of inflammatory factors IL-1β and IL-6 by ELISA, as well as expression of pAKT and AKT by western blot. Compared with control group, miR-184 and pAKT expression was significantly increased in the HS group. Transfection of miR-184 siRNA into Fb significantly downregulated miR-184 expression, inhibited cell proliferation, promoted Caspase 3 activity, decreased IL-1β and IL-6 secretion, and reduced pAKT level (P < 0.05). miR-184 expression is increased in hypertrophic scar tissue. Down-regulation of miR-184 expression in proliferative scar tissue fibroblasts can down-regulate PI3K/AKT signaling pathway, inhibit inflammation, promote apoptosis, inhibit fibroblast proliferation, and regulate hypertrophic scar formation.

miR-486-3p Controls the Apoptosis of Endometrial Carcinoma Cells

2022 ◽  
Vol 12 (5) ◽  
pp. 1002-1007
Author(s):  
Donghua Wang ◽  
Xiaoli Liu ◽  
Lirong Cao ◽  
Shixiong Gong ◽  
Yi He ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Endometrial Carcinoma ◽  
Real Time ◽  
Spectrophotometric Method ◽  
Real Time Pcr ◽  
Carcinoma Cells ◽  
Migration And Invasion ◽  
Invasive Capacity ◽  
Ec Cells

Our study aimed to discuss the mechanism of miR-486-3p in controlling the apoptosis of endometrial carcinoma (EC) cells. EC cells were divided into NC group, miR-486-3p mimic and miR-486-3p inhibitor group followed by analysis of miR-486-3p level by Real-time PCR, cell proliferation by spectrophotometric method, apoptosis by FCM, cell migration and invasion by Transwell analysis. EC cells showed reduced miR-486-3p level. The EC malignant biological behaviors could be prompted through retraining miR-486-3p level with increased EC cell invasive capacity. DDR1 was a target of miR-486-3p. The variation of tumor activity could be regulated through controlling DDR1 expression. In conclusion, the apoptotic and invasive characteristic of EC cells are restrained after overexpression of miR-486-3p in EC cells through targeting DDR1, indicating that miR-486-3p could be considered to be one kind of brand-new target for the treatment of EC.

scholarly journals MiR-501 promotes tumor proliferation and metastasis by targeting HOXD10 in endometrial cancer

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
Xiaomei Sun ◽  
Lingtong Hou ◽  
Chunping Qiu ◽  
Beihua Kong
Keyword(s):  
Endometrial Cancer ◽  
Real Time ◽  
Real Time Pcr ◽  
Tumor Formation ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
High Grade ◽  
Quantitative Real Time Pcr ◽  
Proliferation And Metastasis

Abstract Background Several studies have shown the crucial role of miR-501 in regulating cellular pathology in various cancers. However, the function and expression of miR-501 in endometrial cancer (EC) remain obscure. Methods The expression of miR-501 was determined using quantitative real-time PCR. MTT assay, colony formation assay and cell cycle analysis were used to evaluate the proliferation ability. Migration and invasion were assessed using transwell assay. Tumor formation in nude mice was used to observe the effects of miR-501 on cell proliferation and migration in vivo. Luciferase assay, quantitative real-time PCR and western blot were applied to determine that HOXD10 was the target gene of miR-501. Results In this study, we observed significantly up-regulated expression of miR-501 in endometrial cancer, which correlated with higher pelvic lymph node metastasis and shorter overall survival in high-grade endometrial cancer. High expression of miR-501 was also found in the copy-number-high group than other groups. Moreover, in vitro and in vivo assay showed that overexpression of miR-501 can promote proliferation and metastasis. Mechanistically, we found that miR-501 promotes tumor progression by directly targeting HOXD10. Further study also indicated that miR-501 overexpression can activate the AKT/mTOR pathway. Conclusions MiR-501, which functions as an oncomir in endometrial cancer, might be a potential therapeutic target in high grade endometrial cancer.

scholarly journals SETDB1 promotes glioblastoma growth via CSF-1-dependent macrophage recruitment by activating the AKT/mTOR signaling pathway

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Shuai Han ◽  
Wei Zhen ◽  
Tongqi Guo ◽  
Jianjun Zou ◽  
Fuyong Li
Keyword(s):  
Cell Proliferation ◽  
Tumor Microenvironment ◽  
Real Time ◽  
Western Blotting ◽  
Real Time Pcr ◽  
Migration And Invasion ◽  
Common Disease ◽  
High Morbidity ◽  
Macrophage Recruitment ◽  
Syngeneic Mouse Model

Abstract Background Glioblastoma is a common disease of the central nervous system (CNS), with high morbidity and mortality. In the infiltrate in the tumor microenvironment, tumor-associated macrophages (TAMs) are abundant, which are important factors in glioblastoma progression. However, the exact details of TAMs in glioblastoma progression have yet to be determined. Methods The clinical relevance of SET domain bifurcated 1 (SETDB1) was analyzed by immunohistochemistry, real-time PCR and Western blotting of glioblastoma tissues. SETDB1-induced cell proliferation, migration and invasion were investigated by CCK-8 assay, colony formation assay, wound healing and Transwell assay. The relationship between SETDB1 and colony stimulating factor 1 (CSF-1), as well as TAMs recruitment was examined by Western blotting, real-time PCR and syngeneic mouse model. Results Our findings showed that SETDB1 upregulated in glioblastoma and relative to poor progression. Gain and loss of function approaches showed the SETDB1 overexpression promotes cell proliferation, migration and invasion in glioblastoma cells. However, knockdown SETDB1 exerted opposite effects in vitro. Moreover, SETDB1 promotes AKT/mTOR-dependent CSF-1 induction and secretion, which leads to macrophage recruitment in the tumor, resulted in tumor growth. Conclusion Our research clarified that SETDB1 regulates of tumor microenvironment and hence presents a potential therapeutic target for treating glioblastoma.

scholarly journals Biological evaluation of transdichloridoplatinum( II) complexes with 3- and 4-acetylpyridine in comparison to cisplatin

2013 ◽  
Vol 47 (4) ◽  
pp. 346-357 ◽  
Author(s):  
Lana Filipovic ◽  
Sandra Arandelovic ◽  
Nevenka Gligorijevic ◽  
Ana Krivokuca ◽  
Radmila Jankovic ◽  
...  
Keyword(s):  
Western Blot ◽  
Mrna Expression ◽  
Real Time ◽  
Real Time Pcr ◽  
Inductively Coupled Plasma ◽  
Gelatin Zymography ◽  
Biological Evaluation ◽  
Emission Spectrometry ◽  
Quantitative Real Time Pcr

Abstract Background. In our previous study we reported the synthesis and cytotoxicity of two trans-platinum(II) complexes: trans-[PtCl2(3-acetylpyridine)2] (1) and trans-[PtCl2(4-acetylpyridine)2] (2), revealing significant cytotoxic potential of 2. In order to evaluate the mechanism underlying biological activity of both trans-Pt(II) isomers, comparative studies versus cisplatin were performed in HeLa, MRC-5 and MS1 cells. Materials and methods. The cytotoxic activity of the investigated complexes was determined using SRB assay. The colagenolytic activity was determined using gelatin zymography, while the effect of platinum complexes on matrix metalloproteinases 2 and 9 mRNA expression was evaluated by quantitative real-time PCR. Apoptotic potential and cell cycle alterations were determined by FACS analyses. Western blot analysis was used to evaluate the effect on expression of DNA-repair enzyme ERCC1, and quantitative real-time PCR was used for the ERCC1 mRNA expression analysis. In vitro antiangiogenic potential was determined by tube formation assay. Platinum content in intracellular DNA and proteins was determined by inductively coupled plasma-optical emission spectrometry. Results. Compound 2 displayed an apparent cytoselective profile, and flow cytometry analysis in HeLa cells indicated that 2 exerted antiproliferative effect through apoptosis induction, while 1 induced both apoptosis and necrosis. Action of 1 and 2, as analyzed by quantitative real-time PCR and Western blot, was associated with down-regulation of ERCC1. Both trans-complexes inhibited MMP-9 mRNA expression in HeLa, while 2 significantly abrogated in vitro tubulogenesis in MS1 cells. Conclusions. The ability of 2 to induce multiple and selective in vitro cytotoxic effects encourages further investigations of trans-platinum(II) complexes with substituted pyridines.

SRY-Box Transcription Factor 9 (SOX9) Affects the Proliferation, Invasion and Epithelial to Mesenchymal Transition (EMT) of Intrahepatic Cholangiocarcinoma by Regulating Transforming Growth Factor β (TGFβ)/Smad Signaling

2021 ◽  
Vol 11 (10) ◽  
pp. 1891-1899
Author(s):  
Ling Dai ◽  
Yuqing Lu ◽  
Lu Jiang ◽  
Liping Zhu ◽  
Jing Zhang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Western Blot ◽  
Real Time ◽  
Intrahepatic Cholangiocarcinoma ◽  
Real Time Pcr ◽  
Migration And Invasion ◽  
Sox9 Expression ◽  
Smad Signaling ◽  
Tumor Tissues ◽  
E Cadherin

Intrahepatic cholangiocarcinoma (ICC) develops rapidly with a high malignancy. SOX9 expression is increased in several tumors. However, its expression and role in intrahepatic cholangiocarcinoma have not yet been elucidated. Real time PCR and Western blot were done to assess SOX9 expression in tumor tissues and adjacent tissues of ICC. ICC cell line QBC939 cells were separated into control group, SOX9 overexpression group and SOX9 siRNA group followed by analysis of cell survival by MTT assay, cell migration by cell scratch assay, cell invasion by transwell chamber, E-cadherin and Vimentin level by western blot, TGFβ/Smad signaling protein level by real time PCR. SOX9 level in tumor tissues was significantly increased compared to adjacent tissues (P < 0.05) and it was associated with TNM stage, tissue type and metastasis, and survival time (P < 0.05). Transfection of pcDNA3.1-SOX9 upregulated SOX9, promoted cell proliferation, migration and invasion, downregulated E-cadherin, upregulated Vimentin, TGF-β1 and Smad4 (P < 0.05). SOX9 siRNA transfection into QBC939 cells could significantly reverse the above mentioned changes (P < 0.05). SOX9 level is increased in intrahepatic cholangiocarcinoma and targeting SOX9 can inhibit cell migration and invasion, and EMT via regulating TGFβ/Smad signaling.

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