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  • S. Karger AG  (11)
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  • Pharmacy  (11)
  • 1
    Online Resource
    Online Resource
    MEGF6 Promotes the Epithelial-to-Mesenchymal Transition via the TGFβ/SMAD Signaling Pathway in Colorectal Cancer Metastasis
    S. Karger AG ; 2018
    In:  Cellular Physiology and Biochemistry Vol. 46, No. 5 ( 2018), p. 1895-1906
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 46, No. 5 ( 2018), p. 1895-1906
    Abstract: Background/Aims: Colorectal cancer (CRC) is a malignancy that has high morbidity and mortality and is initiated from accumulative genetic events. Although much effort has been made to elucidate the genetic mechanism underlying this disease, it still remains unknown. Here, we discovered a novel role for multiple epidermal growth factor-like domains protein 6 (MEGF6) in CRC, namely, that it induces the epithelial-to-mesenchymal transition (EMT) to promote CRC metastasis via the transforming growth factor beta (TGFβ)/SMAD signaling pathway. Methods: RNA sequencing data from the Gene Expression Omnibus database were analyzed using R software. Based on The Cancer Genome Atlas Colon Adenocarcinoma (TCGA-COAD) cohort, the clinical significance of MEGF6 was investigated. HCT8R, HCT116, and LoVo CRC cells were transfected with small interfering RNA against MEGF6, and their proliferation and sensitivity to fluorouracil were evaluated with the MTT cell proliferation and colony formation assays. Proteins associated with cell growth were detected by western blot analysis. The apoptosis of cells was evaluated by Annexin V/propidium iodide staining, and transwell assays were performed to assess the involvement of MEGF6 in cell migration. Markers of EMT and TGFβ/SMAD signaling were evaluated by quantitative PCR and western blotting, and the correlation between MEGF6 and these markers was assessed in the TCGA colon and renal adenocarcinoma cohort. Results: The results showed that MEGF6 was upregulated in HCT8R cells. In addition, MEGF6 was significantly overexpressed in tumor tissue and predicted a poor survival in the TCGA-COAD cohort. Moreover, MEGF6 accelerated CRC cell growth and inhibited apoptosis, and promoted CRC metastasis by inducing the EMT. Finally, we found that TGFβ/SMAD signaling triggered the expression of Slug, which regulates the MEGF6-mediated EMT. Conclusions: MEGF6 may serve as an oncogene to promote cell proliferation and inhibit apoptosis. MEGF6 can also accelerate cell migration via TGFβ/SMAD signaling-mediated EMT.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000489374
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
    detail.hit.zdb_id: 1482056-0
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  • 2
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    Online Resource
    Valsartan Reduced Atrial Fibrillation Susceptibility by Inhibiting Atrial Parasympathetic Remodeling through MAPKs/Neurturin Pathway
    S. Karger AG ; 2015
    In:  Cellular Physiology and Biochemistry Vol. 36, No. 5 ( 2015), p. 2039-2050
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 36, No. 5 ( 2015), p. 2039-2050
    Abstract: Background/Aims: Angiotensin II receptor blockers (ARBs) have been proved to be effective in preventing atrial structural and electrical remodelinq in atrial fibrillation (AF). Previous studies have shown that parasympathetic remodeling plays an important role in AF. However, the effects of ARBs on atrial parasympathetic remodeling in AF and the underlying mechanisms are still unknown. Methods: Canines were divided into sham-operated, pacing and valsartan + pacing groups. Rats and HL-1 cardiomyocytes were divided into control, angiotensin II (Ang II) and Ang II + valsartan groups, respectively. Atrial parasympathetic remodeling was quantified by immunocytochemical staining with anti-choline acetyltransferase (ChAT) antibody. Western blot was used to analysis the protein expression of neurturin. Results: Both inducibility and duration were increased in chronic atrial rapid-pacing canine model, which was significantly inhibited by the treatment with valsartan. The density of ChAT-positive nerves and the protein level of neurturin in the atria of pacing canines were both increased than those in sham-operated canines. Ang II treatment not only induced atrial parasympathetic remodeling in rats, but also up-regulated the protein expression of neurturin. Valsartan significantly prevented atrial parasympathetic remodeling, and suppressed the protein expression of neurturin. Meanwhile, valsartan inhibited Ang II -induced up-regulation of neurturin and MAPKs in cultured cardiac myocytes. Inhibition of MAPKs dramatically attenuated neurturin up-regulation induced by Ang II. Conclusion: Parasympathetic remodeling was present in animals subjected to rapid pacing or Ang II infusion, which was mediated by MAPKs/neurturin pathway. Valsartan is able to prevent atrial parasympathetic remodeling and the occurrence of AF via inhibiting MAPKs/neurturin pathway.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000430171
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2015
    detail.hit.zdb_id: 1482056-0
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  • 3
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    Online Resource
    The Different Induction Mechanisms of Growth Arrest DNA Damage Inducible Gene 45 β in Human Hepatoma Cell Lines
    S. Karger AG ; 2012
    In:  Chemotherapy Vol. 58, No. 2 ( 2012), p. 165-174
    Details
    In: Chemotherapy, S. Karger AG, Vol. 58, No. 2 ( 2012), p. 165-174
    Abstract: 〈 b 〉 〈 i 〉 Aims: 〈 /i 〉 〈 /b 〉 Downregulation of the growth arrest and DNA damage-inducible gene 45 β (GADD45β) has been verified to be specific to HCC and consistent with the degree of malignancy. The differences in induction mechanisms of GADD45β were investigated based on transcriptional regulation. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Following our published data from S-adenosylmethionine (SAMe), oxaliplatin and sorafenib were further used to stimulate GADD45β expression in cultured HepG2 ( 〈 i 〉 p53 〈 /i 〉 wild type) and Hep3B ( 〈 i 〉 p53 〈 /i 〉 null) hepatoma cells in vitro. The different effects on cell viability, DNA synthesis and caspase activities were also measured. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Oxaliplatin and sorafenib could induce GADD45β in both HepG2 and Hep3B in a dose-dependent manner with rapid and direct cytotoxic effect. Transcriptional activity of NF-ĸB and E2F-1 were both enhanced by oxaliplatin and sorafenib. However, SAMe could only induce GADD45β in HepG2 through the NF-ĸB pathway, resulting in a slow and indirect cytotoxic effect. Although all three inducers could lead to a pronounced rise in caspase activities, only high concentration of SAMe could inhibit DNA synthesis as significantly as the chemo drugs. No apparent changes in GADD45β induction, promoter activity or cytotoxic effects were observed in Hep3B 〈 sup 〉 +p53 〈 /sup 〉 when treated with oxaliplatin and sorafenib, while relatively significant changes occurred with SAMe. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 GADD45β induction is a novel mechanism of SAMe-mediated hepatoprotection with 〈 i 〉 p53 〈 /i 〉 involvement.
    Type of Medium: Online Resource
    ISSN: 0009-3157 , 1421-9794
    URL: Article
    DOI: 10.1159/000338386
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2012
    detail.hit.zdb_id: 1482111-4
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  • 4
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    Actein Antagonizes Oral Squamous Cell Carcinoma Proliferation through Activating FoxO1
    S. Karger AG ; 2021
    In:  Pharmacology Vol. 106, No. 9-10 ( 2021), p. 551-563
    Details
    In: Pharmacology, S. Karger AG, Vol. 106, No. 9-10 ( 2021), p. 551-563
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Oral squamous cell carcinoma (OSCC) is among the most prevalent head and neck malignancies globally, and it is associated with high mortality rates. Actein is one of the primary active components extractable from the rhizomes of 〈 i 〉 Cimicifuga foetida 〈 /i 〉 . This study aimed to evaluate the anti-OSCC effects of actein and evaluate the potential underlying mechanisms. 〈 b 〉 〈 i 〉 Methods and Results: 〈 /i 〉 〈 /b 〉 CCK-8 cell proliferation experiments demonstrated significant dose- and time-dependent anti-OSCC effects of actein, while actein had weak cytotoxic effects on normal oral cell lines. Flow cytometry for cell cycle evaluation revealed that actein could induce cell cycle arrest at the G1 phase among OSCC cell lines. In our Annexin V/PI double staining apoptosis analysis, actein induced significant apoptosis among OSCC cells, with upregulation of Bax and downregulation of Bcl-2. Our mechanistic study implicated the involvement of the Akt/FoxO1 pathway in the anti-OSCC effects of actein. Akt1 and Akt2 expression significantly decreased in association with the FoxO1 upregulation. Furthermore, Bim and p21 were significantly upregulated, while survivin expression was downregulated. Finally, actein treatment was associated with significant p-Akt downregulation and p-FoxO1 upregulation in OSCC cells, demonstrating the validated roles of Akt/FoxO1 in actein-mediated OSCC cell apoptosis and cell cycle arrest. FoxO1 knockdown significantly reversed the anti-OSCC effects of actein. Additionally, a xenograft model indicated that actein could inhibit OSCC cell growth in vivo. 〈 b 〉 〈 i 〉 Conclusions: 〈 /i 〉 〈 /b 〉 Our findings demonstrated that actein could be a strong anti-OSCC candidate. Further evaluations of its safety and effectiveness are necessary before it can be considered for clinical use.
    Type of Medium: Online Resource
    ISSN: 0031-7012 , 1423-0313
    URL: Article
    DOI: 10.1159/000515601
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2021
    detail.hit.zdb_id: 1483550-2
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  • 5
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    Liver Plays a Major Role in FGF-21 Mediated Glucose Homeostasis
    S. Karger AG ; 2018
    In:  Cellular Physiology and Biochemistry Vol. 45, No. 4 ( 2018), p. 1423-1433
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 45, No. 4 ( 2018), p. 1423-1433
    Abstract: Background/Aims: The liver is a vital organ in vertebrates and has a wide range of functions, including glucose absorption, glycogen storage and glucose production. Fibroblast growth factor (FGF)-21 is a metabolic regulator that is primarily produced by the liver. In this paper, we studied the effect of FGF-21 on glucose metabolism in the liver. Methods: The glucose uptake of cells was detected by 2-Deoxy-d-[3H] glucose; the synergy between insulin and FGF-21 was evaluated. The mRNA expression of GLUT1-4, G6Pase and PEPCK was detected by real-time PCR. Glycogen synthesis was examined by the anthrone method. Blood samples to monitor glucose in db/db diabetic mice were obtained by tail snip. Glucose metabolism in the liver and adipose tissues was observed by fluorescence microscopy. Results: In this study, FGF-21 stimulated glucose uptake by liver cells in both a dose and time-dependent manner, and at the same time, FGF-21 specifically stimulated GLUT1 expression in the liver cells. Furthermore, FGF-21 demonstrated a synergistic effect with insulin on glucose absorption, which is in accordance with enhanced GLUT-1 and -4 expression. Treatment with FGF-21 increased glycogen storage in liver cells. Consistent with in vitro results, FGF-21 lowered the plasma glucose level and stimulated GLUT1 expression and glycogen synthesis in db/db diabetic mice. Simultaneously, FGF-21 inhibited the gene expression of G6Pase and PEPCK. Conclusion: Our results suggest that FGF-21 clears up plasma glucose by stimulating glucose absorption in the liver of diabetic animals and decreases glucose release from the liver by inhibiting gluconeogenesis. Overall, these data indicate that the liver is an important target organ of FGF-21 to regulate glucose metabolism.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000487568
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
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  • 6
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    The Long Noncoding RNA, Growth Arrest-Specific 5, Suppresses Gastric Cancer by Downregulating miR-21 Expression
    S. Karger AG ; 2020
    In:  Pharmacology Vol. 105, No. 7-8 ( 2020), p. 434-444
    Details
    In: Pharmacology, S. Karger AG, Vol. 105, No. 7-8 ( 2020), p. 434-444
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Gastric cancer has become the second major cause of cancer death. The aim of the present study was to explore the relationship between miR-21 and the long noncoding RNA growth arrest-specific 5 (GAS5) in gastric cancer and the effect on gastric cancer cells. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 The expression of miR-21 and GAS5 mRNA was analyzed by quantitative real-time-PCR. Overexpression of GAS5 was used to investigate the biological functions of GAS5 in cells. The cell proliferation was detected by cell counting kit-8 assay and the cell migration and invasion were detected by Transwell. Cell apoptosis was evaluated by Annexin V-FITC/PI staining and apoptosis-related proteins were detected by western blot. The mechanism of GAS5 in vivo was evaluated by the tumorigenesis of nude mice, and dual luciferase reporter was used to determine if miR-21 is a GAS5 target. The inhibition of miR-21 and the simultaneous overexpression of GAS5 and miR-21 were further performed, and the above indicators were detected again. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 GAS5 was low expression and miR-21 was high expression in gastric cancer tissues and cells. GAS5 overexpression reduced the proliferation, migration, and invasion of gastric cancer cells and increased the apoptosis of gastric cancer cells. The growth rate of GAS5 group slowed down and the volume of tumor decreased. miR-21 is a GAS5 target and GAS5 inhibits the proliferation of gastric cancer cells by targeting miR-21. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 Our research shown that overexpression of GAS5 can significantly inhibit the proliferation, migration, invasion and tumor formation of gastric cancer cells, and promote the apoptosis of gastric cancer cells, which may be related to the targeting inhibition of miR-21 expression by GAS5.
    Type of Medium: Online Resource
    ISSN: 0031-7012 , 1423-0313
    URL: Article
    DOI: 10.1159/000504674
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2020
    detail.hit.zdb_id: 1483550-2
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  • 7
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    NEDD4 Depletion Inhibits Hepatocellular Carcinoma Growth via Targeting PTEN
    S. Karger AG ; 2016
    In:  Cellular Physiology and Biochemistry Vol. 39, No. 2 ( 2016), p. 768-779
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 39, No. 2 ( 2016), p. 768-779
    Abstract: Background/Aims: Neural precursor cell-expressed developmentally down-regulated gene 4 (NEDD4) plays an important role in tumor cell growth, yet its role in hepatocellular carcinoma (HCC) remains unclear. This study is to establish NEDD4 as a prognostic biomarker by which the survival of HCC patients can be predicted and to reveal the role of NEDD4 in hepatocellular carcinoma cell growth. Methods: The expression of NEDD4 in 219 HCC specimens was assessed by immunohistochemistry. Postoperative overall survival and time to recurrence were evaluated by univariate and multivariate analyses. The roles of NEDD4 in hepatocellular carcinoma cell proliferation and invasion were determined. Results: The patients with low NEDD4 expression tumors had an average cumulative survival of 64.9 ± 6.5 months during follow-up while the patients with high NEDD4 expression tumors had an average cumulative survival of 20.3 ± 15.8 months. NEDD4 silencing inhibited Huh7 cell proliferation and altered cell cytoskeletal assembly, and NEDD4 depletion furthermore seemed to suppress cell migration and invasion. A possible molecular mechanism for the observed effects might be that NEDD4 silence led to an increase in PTEN (phosphatase and tensin homologue) expression, which in turn resulted in the inactivation of STAT3, AKT, and ERK1/2. Conclusion: Our findings indicate that NEDD4 may participate in the HCC progression and may therefore be a potential target for HCC therapy.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000445667
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2016
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  • 8
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    Endothelial Cells Promote Calcification in Aortic Smooth Muscle Cells from Spontaneously Hypertensive Rats
    S. Karger AG ; 2018
    In:  Cellular Physiology and Biochemistry Vol. 49, No. 6 ( 2018), p. 2371-2381
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 49, No. 6 ( 2018), p. 2371-2381
    Abstract: Background/Aims: Vascular calcification and hypertension are intimately linked, and the progression of hypertension is closely correlated with endothelial dysfunction. However, the role of endothelial cells (ECs) in vascular calcification of hypertension remains unclear. Therefore, the present study explored the effects of ECs on calcification of smooth muscle cells (SMCs) from aortas of spontaneously hypertensive rats (SHR). Methods: Aortic ECs and SMCs were isolated from SHR and Wistar rats, respectively. The roles of ECs in the regulation of SMCs calcification were investigated by co-culture and conditioned culture model. Calcium deposition of SMCs was detected by von Kossa staining. Quantization of calcium content in SMCs was determined colorimetrically by the o-cresolphthalein complexone method. Alkaline phosphatase (ALP) activity was measured colorimetrically by p-nitrophenol. The expression levels of MMP-2, MMP-9 and the calcification-promoting proteins were analyzed by Western blot. Results: Calcium deposition, ALP activity and the expression levels of calcification-promoting proteins in SMCs of SHR were significantly higher than that cultured without ECs after 6 days of co-culture with ECs or conditioned culture with the medium of ECs, however, there were no statistical differences between SMCs of Wistar rats. MMP-2 and MMP-9 in co-cultured ECs from SHR were dramatically higher than that cultured without SMCs, nevertheless, there were no statistical differences between ECs from Wistar rats and between SMCs from SHR or Wistar rats. Moreover, SB-3CT, a specific inhibitor of gelatinases, decreased calcium content and the expression levels of calcification-promoting proteins in both co-cultured and conditionally cultured SMCs from SHR. Conclusion: ECs have the ability to promote calcification of aortic SMCs of SHR, and elevated expressions of MMP-2 and MMP-9 in ECs of SHR might facilitate the calcification of SMCs.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000493837
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
    detail.hit.zdb_id: 1482056-0
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  • 9
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    Tip60 Suppresses Cholangiocarcinoma Proliferation and Metastasis via PI3k-AKT
    S. Karger AG ; 2018
    In:  Cellular Physiology and Biochemistry Vol. 50, No. 2 ( 2018), p. 612-628
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 50, No. 2 ( 2018), p. 612-628
    Abstract: Background/Aims: Aberrant expression of Tip60 is associated with progression in many cancers. However, the role of Tip60 in cancer progression remains contradictory. The aim of this study was to investigate the clinical significance, biological functions and underlying mechanisms of Tip60 deregulation in cholangiocarcinoma (CCA) for the first time. Methods: Quantitative real-time PCR (QRT-PCR), western blotting and immunohistochemistry staining (IHC) were carried out to measure Tip60 expression in CCA tissues and cell lines. Kaplan–Meier analysis and the log-rank test were used for survival analysis. In vitro, cell proliferation was evaluated by flow cytometry and CCK-8, colony formation, and EDU assays. Migration/ invasion was evaluated by trans-well assays. Phosphokinase array was used to confirm the dominant signal regulated by Tip60. Tumor growth and metastasis were demonstrated in vivo using a mouse model. Results: Tip60 was notably downregulated in CCA tissues, which was associated with greater tumor size, venous invasion, and TNM stage. Down-regulation of Tip60 was associated with tumor progression and poorer survival in CCA patients. In vitro and in vivo studies demonstrated that Tip60 suppressed growth and metastasis throughout the progression of CCA. We further identified the PI3K/AKT pathway as a dominant signal of Tip60 and suggested that Tip60 regulated CCA cell proliferation and metastasis via PT3K-AKT pathway. Pearson analysis revealed that PTEN was positively correlated with the Tip60 level in CCA tissues. Conclusion: Tip60, as a tumor suppressor in CCA via the PI3K/AKT pathway, might be a promising therapeutic target or prognostic marker for CCA.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000494183
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
    detail.hit.zdb_id: 1482056-0
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  • 10
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    MiR-193a-3p is an Important Tumour Suppressor in Lung Cancer and Directly Targets KRAS
    S. Karger AG ; 2017
    In:  Cellular Physiology and Biochemistry Vol. 44, No. 4 ( 2017), p. 1311-1324
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 44, No. 4 ( 2017), p. 1311-1324
    Abstract: Background/Aims: MicroRNAs (miRNAs) have emerged as major regulators of tumour development and progression in non-small cell lung cancer (NSCLC). However, the role of miR-193a-3p in NSCLC is still unclear. Methods: Quantitative RT-PCR was used to detect miR-193a-3p expression levels in NSCLC tumour tissues. CCK8, EdU and cell migration assays were performed to analyse the biological functions of miR-193a-3p in NSCLC cells. Luciferase reporter assays were used to validate the bioinformatics-predicted target genes of miR-193a-3p. Western blotting and RNA/DNA interference carried out to evaluate the association between miR-193a-3p and KRAS. Results: miR-193a-3p expression was decreased in the NSCLC tumour tissues. We investigated the biological effects of miR-193a-3p both in vivo and in vitro and found that enforced expression of miR-193a-3p inhibited tumour formation and suppressed cell proliferation and cell migration. KRAS was found to be a potential target of miR-193a-3p, and dual luciferase reporter assays showed that miR-193a-3p directly binds to the 3’-untranslated region (3’-UTR) of KRAS mRNA. In addition, we found that changing the expression of KRAS had the opposite results to those induced by miR-193a-3p in the NSCLC cells. Importantly, simultaneous overexpression of miR-193a-3p and KRAS could counteract the effects of both on cellular functions. Conclusion: These findings highlight an important role for miR-193a-3p as a tumour suppressor in NSCLC pathogenesis via the regulation of KRAS expression.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000485491
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2017
    detail.hit.zdb_id: 1482056-0
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