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Pesquisa : D08.811.913.696.620.500 [Categoria DeCS]
Referências encontradas : 25 [refinar]
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  1 / 25 LILACS  
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Id: biblio-1132511
Autor: Peng, Bing; Li, Chao; He, Lili; Tian, Mi; Li, Xin.
Título: miR-660-5p promotes breast cancer progression through down-regulating TET2 and activating PI3K/AKT/mTOR signaling
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;53(12):e9740, 2020. tab, graf.
Idioma: en.
Projeto: EGFR.
Resumo: Breast cancer (BC) is a commonly diagnosed cancer in females. MicroRNA-660-5p (miR-660-5p) has been reported to be involved in the occurrence and development of BC. However, the regulatory network of miR-660-5p in BC has not been fully addressed. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the enrichment of miR-660-5p and tet-eleven translocation 2 (TET2) in BC tissues and cells. Cell counting kit-8 (CCK8), flow cytometry, and transwell migration and invasion assays were used to measure cell proliferation, apoptosis, migration, and invasion. The target relationship between miR-660-5p and TET2 was confirmed by dual luciferase reporter assay. Protein expression was measured by western blot. The expression of miR-660-5p was elevated in BC, and high expression of miR-660-5p was closely related to lymph node metastasis, advanced TNM stage, and vascular invasion of BC tumors. miR-660-5p silencing inhibited cell proliferation and metastasis, but induced apoptosis of BC cells. TET2 was identified as a direct target of miR-660-5p, and the interference of TET2 partly reversed the suppressive effects of miR-660-5p silencing on the malignant potential of BC cells. miR-660-5p promoted BC progression partly through modulating TET2 and PI3K/AKT/mTOR signaling. miR-660-5p/TET2 axis might be a promising target for BC treatment.
Descritores: Neoplasias da Mama/genética
MicroRNAs/genética
-Transdução de Sinais
Proteínas Proto-Oncogênicas
Fosfatidilinositol 3-Quinases/genética
Linhagem Celular Tumoral
Proteínas de Ligação a DNA
Proteínas Proto-Oncogênicas c-akt/genética
Serina-Treonina Quinases TOR/genética
Limites: Humanos
Feminino
Responsável: BR1.1 - BIREME


  2 / 25 LILACS  
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Id: biblio-1055491
Autor: Xing, Xiaowei; Guo, Shuang; Zhang, Guanghao; Liu, Yusheng; Bi, Shaojie; Wang, Xin; Lu, Qinghua.
Título: miR-26a-5p protects against myocardial ischemia/reperfusion injury by regulating the PTEN/PI3K/AKT signaling pathway
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;53(2):e9106, 2020. graf.
Idioma: en.
Projeto: Youth Fund of the Second Hospital of Shandong University, China; . Key Research and Development Project in Shandong, China; . Health Science and Technology Development Program Project, China; . Shandong Provincial Natural Science Foundation, China.
Resumo: Reperfusion strategies in acute myocardial infarction (AMI) can cause a series of additional clinical damage, defined as myocardial ischemia/reperfusion (I/R) injury, and thus there is a need for effective therapeutic methods to attenuate I/R injury. miR-26a-5p has been proven to be an essential regulator for biological processes in different cell types. Nevertheless, the role of miR-26a-5p in myocardial I/R injury has not yet been reported. We established an I/R injury model in vitro and in vivo. In vitro, we used cardiomyocytes to simulate I/R injury using hypoxia/reoxygenation (H/R) assay. In vivo, we used C57BL/6 mice to construct I/R injury model. The infarct area was examined by TTC staining. The level of miR-26a-5p and PTEN was determined by bioinformatics methods, qRT-PCR, and western blot. In addition, the viability and apoptosis of cardiomyocytes were separately detected by MTT and flow cytometry. The targeting relationship between miR-26a-5p and PTEN was analyzed by the TargetScan website and luciferase reporter assay. I/R and H/R treatment induced myocardial tissue injury and cardiomyocyte apoptosis, respectively. The results showed that miR-26a-5p was down-regulated in myocardial I/R injury. PTEN was found to be a direct target of miR-26a-5p. Furthermore, miR-26a-5p effectively improved viability and inhibited apoptosis in cardiomyocytes upon I/R injury by inhibiting PTEN expression to activate the PI3K/AKT signaling pathway. miR-26a-5p could protect cardiomyocytes against I/R injury by regulating the PTEN/PI3K/AKT pathway, which offers a potential approach for myocardial I/R injury treatment.
Descritores: Traumatismo por Reperfusão Miocárdica/metabolismo
Isquemia Miocárdica/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Miócitos Cardíacos/patologia
MicroRNAs/metabolismo
PTEN Fosfo-Hidrolase/metabolismo
-Transdução de Sinais
Western Blotting
Modelos Animais de Doenças
Proteínas Proto-Oncogênicas c-akt/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Citometria de Fluxo
Camundongos Endogâmicos C57BL
Limites: Animais
Coelhos
Responsável: BR1.1 - BIREME


  3 / 25 LILACS  
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Id: biblio-1132533
Autor: Bao, H R; Chen, J L; Li, F; Zeng, X L; Liu, X J.
Título: Relationship between PI3K/mTOR/RhoA pathway-regulated cytoskeletal rearrangements and phagocytic capacity of macrophages
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;53(7):e9207, 2020. tab, graf.
Idioma: en.
Projeto: National Natural Science Foundation of China; . Key Research and Development Programs of Gansu Province.
Resumo: The objective of this study was to investigate the relationship between PI3K/mTOR/RhoA signaling regulated cytoskeletal rearrangements and phagocytic capacity of macrophages. RAW264.7 macrophages were divided into four groups; blank control, negative control, PI3K-RNAi, and mTOR-RNAi. The cytoskeletal changes in the macrophages were observed. Furthermore, the phagocytic capacity of macrophages against Escherichia coli is reported as mean fluorescence intensity (MFI) and percent phagocytosis. Transfection yielded 82.1 and 81.5% gene-silencing efficiencies against PI3K and mTOR, respectively. The PI3K-RNAi group had lower mRNA and protein expression levels of PI3K, mTOR, and RhoA than the blank and negative control groups (Р<0.01). The mTOR-RNAi group had lower mRNA and protein levels of mTOR and RhoA than the blank and the negative control groups (Р<0.01). Macrophages in the PI3K-RNAi group exhibited stiff and inflexible morphology with short, disorganized filopodia and reduced number of stress fibers. Macrophages in the mTOR-RNAi group displayed pronounced cellular deformations with long, dense filopodia and an increased number of stress fibers. The PI3K-RNAi group exhibited lower MFI and percent phagocytosis than blank and negative control groups, whereas the mTOR-RNAi group displayed higher MFI and percent phagocytosis than the blank and negative controls (Р<0.01). Before and after transfection, the mRNA and protein levels of PI3K were both positively correlated with mTOR and RhoA (Р<0.05), but the mRNA and protein levels of mTOR were negatively correlated with those of RhoA (Р<0.05). Changes in the phagocytic capacity of macrophages were associated with cytoskeletal rearrangements and were regulated by the PI3K/mTOR/RhoA signaling pathway.
Descritores: Fagocitose/fisiologia
Citoesqueleto/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Proteína rhoA de Ligação ao GTP/metabolismo
Serina-Treonina Quinases TOR/metabolismo
Macrófagos/metabolismo
-Transfecção
Transdução de Sinais
Western Blotting
Inativação Gênica
Interferência de RNA
Reação em Cadeia da Polimerase em Tempo Real
Células RAW 264.7
Vetores Genéticos
Limites: Humanos
Animais
Ratos
Responsável: BR1.1 - BIREME


  4 / 25 LILACS  
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Id: biblio-1132556
Autor: Lv, Fenghua; Wang, Zhuo; Huang, Yanli; Si, Aoyang; Chen, Yulei.
Título: CLEC3B protects H9c2 cardiomyocytes from apoptosis caused by hypoxia via the PI3K/Akt pathway
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;53(9):e9693, 2020. tab, graf.
Idioma: en.
Projeto: First Affiliated Hospital of Xinxiang Medical University.
Resumo: Ischemic heart disease (IHD) is one of the leading causes of death worldwide. C-type lectin domain family 3 member B (CLEC3B) is a C-type lectin superfamily member and is reported to promote tissue remodeling. The serum levels of CLEC3B are downregulated in patients with cardiovascular disease. However, the molecular mechanisms of CLEC3B in IHD is not well-characterized. Therefore, we overexpressed CLEC3B and silenced CLEC3B in H9c2 rat cardiomyocytes for the first time. We then constructed a model of IHD in vitro through culturing H9c2 cardiomyocytes in serum-free medium under oxygen-deficit conditions. Then, Cell Counting Kit-8 (CCK-8), flow cytometry, qRT-PCR, and western blot assays were performed to investigate cell viability, apoptosis, and expression levels of CLEC3B, phosphatidylinositol 3-kinase (PI3K), phosphorylated PI3K (p-PI3K), protein kinase B (Akt), phosphorylated Akt (p-Akt), and cleaved-caspase 3. We observed that the mRNA expression of CLEC3B was decreased in hypoxic H9c2 cardiomyocytes (P<0.05). Overexpression of CLEC3B increased cell viability (P<0.01), inhibited cell apoptosis (P<0.05), upregulated the levels of p-PI3K/PI3K and p-Akt/Akt (P<0.01 or P<0.05), and downregulated expression of cleaved-caspase 3 (P<0.001) in hypoxic H9c2 cardiomyocytes while silencing of CLEC3B caused the opposite results. Inhibition of the PI3K/Akt pathway reversed the protective effect of CLEC3B on hypoxic H9c2 cardiomyocytes. Our study demonstrated that CLEC3B alleviated the injury of hypoxic H9c2 cardiomyocytes via the PI3K/Akt pathway.
Descritores: Apoptose/fisiologia
Lectinas Tipo C/metabolismo
-Transdução de Sinais
Fosfatidilinositol 3-Quinases
Miócitos Cardíacos/fisiologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Fosfatidilinositol 3-Quinase
Hipóxia
Limites: Humanos
Animais
Ratos
Responsável: BR1.1 - BIREME


  5 / 25 LILACS  
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Id: biblio-1153529
Autor: Chen, Dayin; Chen, Tingyu; Guo, Yingxue; Wang, Chennan; Dong, Longxin; Lu, Chunfeng.
Título: Suppressive effect of platycodin D on bladder cancer through microRNA-129-5p-mediated PABPC1/PI3K/AKT axis inactivation
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;54(3):10222-0, 2021. tab, graf.
Idioma: en.
Resumo: Platycodin D (PD) is a major constituent of Platycodon grandiflorum and has multiple functions in disease control. This study focused on the function of PD in bladder cancer cell behaviors and the molecules involved. First, we administered PD to the bladder cancer cell lines T24 and 5637 and the human uroepithelial cell line SV-HUC-1. Cell viability and growth were evaluated using MTT, EdU, and colony formation assays, and cell apoptosis was determined using Hoechst 33342 staining and flow cytometry. The microRNAs (miRNAs) showing differential expression in cells before and after PD treatment were screened. Moreover, we altered the expression of miR-129-5p and PABPC1 to identify their functions in bladder cancer progression. We found that PD specifically inhibited the proliferation and promoted the apoptosis of bladder cancer cells; miR-129-5p was found to be partially responsible for the cancer-inhibiting properties of PD. PABPC1, a direct target of miR-129-5p, was abundantly expressed in T24 and 5637 cell lines and promoted cell proliferation and suppressed cell apoptosis. In addition, PABPC1 promoted the phosphorylation of PI3K and AKT in bladder cancer cells. Altogether, PD had a concentration-dependent suppressive effect on bladder cancer cell growth and was involved in the upregulation of miR-129-5p and the subsequent inhibition of PABPC1 and inactivation of PI3K/AKT signaling.
Descritores: Neoplasias da Bexiga Urinária/genética
Neoplasias da Bexiga Urinária/tratamento farmacológico
-Saponinas
Triterpenos
Regulação Neoplásica da Expressão Gênica
Apoptose
Fosfatidilinositol 3-Quinases/metabolismo
MicroRNAs
Linhagem Celular Tumoral
Proliferação de Células
Proteínas Proto-Oncogênicas c-akt/metabolismo
Limites: Humanos
Responsável: BR1.1 - BIREME


  6 / 25 LILACS  
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Id: biblio-1285670
Autor: Gomes, F G; Almeida, V H; Martins-Cardoso, K; Martins-Dinis, M M D C; Rondon, A M R; Melo, A C de; Tilli, T M; Monteiro, R Q.
Título: Epidermal growth factor receptor regulates fibrinolytic pathway elements in cervical cancer: functional and prognostic implications
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;54(6):e10754, 2021. tab, graf.
Idioma: en.
Projeto: CNPq; . CAPES; . FAPERJ.
Resumo: Epidermal growth factor receptor (EGFR) signaling and components of the fibrinolytic system, including urokinase-type plasminogen activator (uPA) and thrombomodulin (TM), have been implicated in tumor progression. In the present study, we employed cBioPortal platform (http://www.cbioportal.org/), cancer cell lines, and an in vivo model of immunocompromised mice to evaluate a possible cooperation between EGFR signaling, uPA, and TM expression/function in the context of cervical cancer. cBioPortal analysis revealed that EGFR, uPA, and TM are positively correlated in tumor samples of cervical cancer patients, showing a negative prognostic impact. Aggressive human cervical cancer cells (CASKI) presented higher gene expression levels of EGFR, uPA, and TM compared to its less aggressive counterpart (C-33A cells). EGFR induces uPA expression in CASKI cells through both PI3K-Akt and MEK1/2-ERK1/2 downstream effectors, whereas TM expression induced by EGFR was dependent on PI3K/Akt signaling alone. uPA induced cell-morphology modifications and cell migration in an EGFR-dependent and -independent manner, respectively. Finally, treatment with cetuximab reduced in vivo CASKI xenografted-tumor growth in nude mice, and decreased intratumoral uPA expression, while TM expression was unaltered. In conclusion, we showed that EGFR signaling regulated expression of the fibrinolytic system component uPA in both in vitro and in vivo settings, while uPA also participated in cell-morphology modifications and migration in a human cervical cancer model.
Descritores: Neoplasias do Colo do Útero/tratamento farmacológico
Fosfatidilinositol 3-Quinases
-Prognóstico
Movimento Celular
Linhagem Celular Tumoral
Receptores ErbB
Camundongos Nus
Limites: Humanos
Animais
Feminino
Ratos
Responsável: BR1.1 - BIREME


  7 / 25 LILACS  
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Id: biblio-1249332
Autor: Bai, Liang; Luo, Li; Gao, Weicheng; Bu, Chenfeng; Huang, Jianfeng.
Título: miR-182 modulates cell proliferation and invasion in prostate cancer via targeting ST6GALNAC5
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;54(8):e9695, 2021. tab, graf.
Idioma: en.
Resumo: Altered expression of miR-182 has been observed in various types of human cancer. The purpose of this study was to investigate the expression of miR-182 and its role in prostate cancer (PCa). Expression of miR-182 and ST6GALNAC5 in tumor tissues and the Du145 PCa cell line was analyzed. Cell proliferation assay, colony formation assay, transwell assay, and wound healing assay were performed. The impact of miR-182 on tumor growth was investigated using a xenograft model. The results indicated that expression of miR-182 was higher in PCa tissues and cell lines, while ST6GALNAC5 was decreased. Downregulating miR-182 significantly inhibited the capacities of proliferation and invasion of PC3 and Du145 cells. ST6GALNAC5 was demonstrated to be a target of miR-182 by luciferase assay, and western blot results indicated PI3K/Akt pathway was involved in miR-182 associated effects on PC3 and Du145 cells. The animal experiment suggested that knockdown of miR-182 inhibited tumor growth. Our study proved that miR-182 participated in the proliferation and invasion of PCa cells via mediating expression of ST6GALNAC5 and established a miR-182/ST6GALNAC5/PI3K/AKT axis in regulation of tumor progression. Our investigation provided a basis for further exploration of the application of miR-182 or ST6GALNAC5-associated therapies for PCa patients.
Descritores: Neoplasias da Próstata/genética
MicroRNAs/genética
-Sialiltransferases
Regulação Neoplásica da Expressão Gênica
Movimento Celular
Fosfatidilinositol 3-Quinases
Linhagem Celular Tumoral
Proliferação de Células
Limites: Humanos
Animais
Masculino
Responsável: BR1.1 - BIREME


  8 / 25 LILACS  
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Id: biblio-1249337
Autor: Cheng, Zhouyang; Ni, Qingfeng; Qin, Lei; Shi, Yang.
Título: MicroRNA-92b augments sorafenib resistance in hepatocellular carcinoma via targeting PTEN to activate PI3K/AKT/mTOR signaling
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;54(9):e10390, 2021. graf.
Idioma: en.
Resumo: Sorafenib (SOR) resistance is still a significant challenge for the effective treatment of hepatocellular carcinoma (HCC). The mechanism of sorafenib resistance remains unclear. Several microRNAs (miRNAs) have been identified as playing a role in impairing the sensitivity of tumor cells to treatment. We examined the mechanism behind the role of miR-92b in mediating sorafenib resistance in HCC cells. We detected that miR-92b expression was significantly upregulated in SOR-resistant HepG2/SOR cells compared to parental HepG2/WT cells. After transfection with miR-92b inhibitor, the proliferation of HepG2/SOR cells was remarkably weakened and rates of apoptosis significantly increased. PTEN was considered to be a functional target of miR-92b according to a luciferase reporter assay. Knockdown of PTEN significantly impaired the ability of miR-92b inhibitor on increasing sorafenib sensitivity of HepG2/SOR cells. Furthermore, we confirmed by western blotting and immunofluorescence that miR-92b can mediate sorafenib resistance by activating the PI3K/AKT/mTOR pathway in HCC cells by directly targeting PTEN. These findings further validate the mechanism of miR-92b in SOR resistance in HCC treatment.
Descritores: Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/tratamento farmacológico
Resistencia a Medicamentos Antineoplásicos
MicroRNAs/genética
Sorafenibe/farmacologia
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/tratamento farmacológico
-Transdução de Sinais
Regulação Neoplásica da Expressão Gênica
Fosfatidilinositol 3-Quinases/metabolismo
Linhagem Celular Tumoral
Proliferação de Células
PTEN Fosfo-Hidrolase/genética
Serina-Treonina Quinases TOR
Limites: Humanos
Responsável: BR1.1 - BIREME


  9 / 25 LILACS  
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Id: lil-796874
Autor: Dias, Queila Cristina; Nunes, Iseu da Silva; Garcia, Patrick Vianna; Fávaro, Wagner José.
Título: Potential therapeutic strategies for non - muscle invasive bladder cancer based on association of intravesical immunotherapy with P-MAPA and systemic administration of cisplatin and doxorubicin
Fonte: Int. braz. j. urol;42(5):942-954, Sept.-Oct. 2016. tab, graf.
Idioma: en.
Projeto: CNPq-Brazil; . FAPESP-Brazil.
Resumo: ABSTRACT The present study describes the histopathological and molecular effects of P-MAPA (Protein aggregate magnesium-ammonium phospholinoleate-palmitoleate anhydride) intravesical immunotherapy combined with systemic doxorubicin or cisplatin for treatment of non-muscle invasive bladder cancer (NMIBC) in an appropriate animal model. Our results showed an undifferentiated tumor, characterizing a tumor invading mucosa or submucosa of the bladder wall (pT1) and papillary carcinoma in situ (pTa) in the Cancer group. The histopathological changes were similar between the combined treatment with intravesical P-MAPA plus systemic Cisplatin and P-MAPA immunotherapy alone, showing decrease of urothelial neoplastic lesions progression and histopathological recovery in 80% of the animals. The animals treated systemically with cisplatin or doxorubicin singly, showed 100% of malignant lesions in the urinary bladder. Furthemore, the combined treatment with P-MAPA and Doxorubicin showed no decrease of urothelial neoplastic lesions progression and histopathological recovery. Furthermore, Akt, PI3K, NF-kB and VEGF protein levels were significantly lower in intravesical P-MAPA plus systemic cisplatin and in intravesical P-MAPA alone treatments than other groups. In contrast, PTEN protein levels were significantly higher in intravesical P-MAPA plus systemic cisplatin and in intravesical P-MAPA alone treatments. Thus, it could be concluded that combination of intravesical P-MAPA immunotherapy and systemic cisplatin in the NMIBC animal model was effective, well tolerated and showed no apparent signs of antagonism between the drugs. In addition, intravesical P-MAPA immunotherapy may be considered as a valuable option for treatment of BCG unresponsive patients that unmet the criteria for early cystectomy.
Descritores: Neoplasias da Bexiga Urinária/terapia
Carcinoma/terapia
Doxorrubicina/uso terapêutico
Cisplatino/uso terapêutico
Imunoterapia/métodos
Proteínas de Membrana/uso terapêutico
Antineoplásicos/uso terapêutico
-Ratos Endogâmicos F344
Neoplasias da Bexiga Urinária/patologia
Administração Intravesical
Vacina BCG
Carcinoma/patologia
Western Blotting
Reprodutibilidade dos Testes
NF-kappa B/análise
Resultado do Tratamento
Terapia Combinada
Progressão da Doença
Fosfatidilinositol 3-Quinases/análise
Modelos Animais
Fator A de Crescimento do Endotélio Vascular/análise
PTEN Fosfo-Hidrolase/análise
Proteínas Proto-Oncogênicas c-akt/análise
Limites: Animais
Feminino
Tipo de Publ: Estudo de Avaliação
Responsável: BR1.1 - BIREME


  10 / 25 LILACS  
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Id: biblio-1249578
Autor: Xu, Haitao; Miao, Jing; Liu, Shuai; Liu, Hongjian; Zhang, Lianguo; Zhang, Qingguang.
Título: Long non-coding RNA KCNQ1 overlapping transcript 1 promotes the progression of esophageal squamous cell carcinoma by adsorbing microRNA-133b
Fonte: Clinics;76:e2175, 2021. tab, graf.
Idioma: en.
Projeto: Shandong Medical Science and Technology Development Program.
Resumo: OBJECTIVE: The long non-coding RNA (lncRNA) KCNQ1 overlapping transcript 1 (KCNQ1OT1) exerts vital regulatory functions in diverse tumors. However, the biological function of KCNQ1OT1 in esophageal squamous cell carcinoma (ESCC) remains unclear. METHODS: KCNQ1OT1 expression was detected in ESCC tissues using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation, apoptosis, migration, and invasion were detected by the CCK-8 assay, EdU assay, flow cytometry analysis, and Transwell experiments, respectively. Bioinformatics analysis, luciferase reporter experiments, and RNA immunoprecipitation assays were used to predict and validate the regulatory relationships between KCNQ1OT1, microRNA-133b (miR-133b) and epidermal growth factor receptor (EGFR). RESULTS: KCNQ1OT1 expression was remarkably upregulated in ESCC tissues and cell lines. Overexpression of KCNQ1OT1 markedly promoted ESCC cell proliferation, migration, and invasion and enhanced the expression of N-cadherin, MMP-2, and MMP-9, but inhibited apoptosis and E-cadherin expression in ESCC cell lines; KCNQ1OT1 knockdown exerted the opposite effects. KCNQ1OT1 could directly bind to miR-133b and suppress its expression, and miR-133b reversed the effects of KCNQ1OT1 overexpression in ESCC cells. MiR-133b reduced the expression of epidermal growth factor receptor (EGFR); further, KCNQ1OT1 activated the phosphatidylinositol 3-kinase/AKT serine/threonine kinase 1 (PI3K/AKT) signaling pathway by repressing miR-133b repression and indirectly upregulating EGFR. KCNQ1OT1 expression was positively correlated with EGFR mRNA expression and negatively correlated with miR-133b expression. CONCLUSION: KCNQ1OT1 facilitates ESCC progression by sponging miR-133b and activating the EGFR/PI3K/AKT pathway.
Descritores: Neoplasias Esofágicas/genética
MicroRNAs/genética
RNA Longo não Codificante/genética
Carcinoma de Células Escamosas do Esôfago/genética
-Fosfatidilinositol 3-Quinases
Proliferação de Células/genética
Canal de Potássio KCNQ1/genética
Limites: Humanos
Responsável: BR1.1 - BIREME



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