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1.
Eur Rev Med Pharmacol Sci ; 24(9): 4756-4765, 2020 05.
Artigo em Inglês | MEDLINE | ID: mdl-32432739

RESUMO

OBJECTIVE: The aim of this study was to elucidate the role of TPM4 in the progression of hepatocellular carcinoma (HCC), and to explore the potential underlying mechanism by interacting with SUSD2. PATIENTS AND METHODS: TPM4 expression levels in 41 HCC tissues and paracancerous tissues were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The relationship between TPM4 level with the pathological indexes and overall survival of HCC patients was analyzed. TPM4 overexpression and knockdown models were constructed in Bel-7402 and Hep3B cells, respectively. Subsequently, Cell Counting Kit-8 (CCK-8) and transwell assay were conducted to assess the effects of TPM4 on the proliferative and migratory abilities of HCC cells. Dual-Luciferase reporter gene assay was performed to verify the binding relationship between TPM4 and SUSD2. In addition, the xenograft model was conducted in HCC-bearing mice administrated with Hep3B cells in vivo. Finally, the effect of TPM4 on the growth of HCC was explored. RESULTS: TPM4 was significantly upregulated in HCC tissues and cell lines. Higher rates of lymphatic and distant metastasis, as well as worse prognosis, were observed in HCC patients with higher expression level of TPM4. The overexpression of TPM4 significantly enhanced the viability and migration abilities of Bel-7402 cells. However, opposite results were observed after the knockdown of TPM4 in Hep3B cells. SUSD2 was verified to be the target of TPM4 and was negatively regulated by TPM4. SUSD2 was lowly expressed in HCC tissues and cell lines. Meanwhile, SUSD2 was considered to be responsible for TPM4-regulated progression of HCC. In mice administrated with Hep3B, the cells transfected with sh-TPM4, the tumor volume and weight of HCC were markedly reduced when compared with the controls. CONCLUSIONS: TPM4 level is correlated with high rates of lymphatic and distant metastasis, as well as poor prognosis of HCC patients. By negatively targeting SUSD2, TPM4 aggravates the progression of HCC by accelerating the proliferative and migratory abilities of HCC cells.


Assuntos
Carcinoma Hepatocelular/metabolismo , Progressão da Doença , Neoplasias Hepáticas/metabolismo , Glicoproteínas de Membrana/biossíntese , Tropomiosina/biossíntese , Animais , Carcinoma Hepatocelular/patologia , Células Hep G2 , Humanos , Neoplasias Hepáticas/patologia , Masculino , Glicoproteínas de Membrana/antagonistas & inibidores , Camundongos , Camundongos Nus , Ensaios Antitumorais Modelo de Xenoenxerto/métodos
2.
J Phys Condens Matter ; 32(31): 315702, 2020 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-32235052

RESUMO

Topological semimetals (TSMs) present intriguing quantum states and have attracted much attention in recent years because of exhibiting various anomalous magneto-transport phenomena. Theoretical prediction shows that some novel phenomena, such as negative magnetoresistance (MR) and the planar Hall effect (PHE), originate from the chiral anomaly in TSMs. In this work, high-field (33 T) Shubnikov-de Haas (SdH) oscillations are obtained to reveal the topology of PtSn4. Giant PHE and anisotropic magnetoresistance (AMR) are observed in Dirac node arcs of semimetal PtSn4. First, a non-zero transverse voltage can be acquired while tilting the in-plane magnetic field. Moreover, the amplitude of PHE sharply increases at T * ∼ 50 K with decreasing temperature, which is suggested to be related to the Fermi surface reconstruction observed in PtSn4. Subsequently, the field-dependent amplitudes of the PHE show an abnormal behavior around 50 K, which is thought to stem from the complex correlation between the chiral charge and electric one in PtSn4 driving the system into different coupling states due to the complicated band structure. On the other hand, the relative AMR is negative and up to -98% at 8.5 T. Our work proves that the PHE measurements are a convincing transport fingerprint feature to confirm the chiral anomaly in TSMs.

3.
Eur Rev Med Pharmacol Sci ; 23(4): 1600-1609, 2019 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-30840283

RESUMO

OBJECTIVE: Long-noncoding RNAs (lncRNAs) have been recently shown to be involved in the regulation of numerous biological processes including tumor progression. In this study, we aimed to explore the role of lncRNA LINC01503 (LINC01503) in the development and progression of glioma. PATIENTS AND METHODS: Relative levels of LINC01503 were evaluated in tumor tissues from 133 patients with glioma as well as from cultured glioma cell lines. The correlation among LINC01503 levels, pathological types, and survivals of glioma patients were also determined using the Kaplan-Meier method and multivariate analysis. Next, we investigated the effect of LINC01503 on the proliferation, colony formation, apoptosis, migration and invasion in the U251 and LN299 cells. Relative protein expression was analyzed by Western blot assays. RESULTS: We found that LINC01503 expression level was significantly up-regulated in glioma tissue and cells, and that its overexpression was significantly correlated with KPS, tumor size and WHO grade in glioma patients. Kaplan-Meier analysis showed that patients with higher levels of LINC01503 had significantly poorer overall survival and disease-free survival than those with lower expression of this lncRNA in glioma patients. Multivariate analysis further confirmed that LINC01503 is an independent prognostic factor in patients with glioma. Functional assays with in vitro showed that knockdown of LINC01503 in the U251 and LN299 cell lines suppressed cells growth, colony formation, invasion and migration, and promoted apoptosis. Mechanistic investigation showed that LINC01503 can modulate Wnt/ß-catenin signaling, as determined by that knockdown of LINC01503 decreased the TOP-FLASH activity and ß-catenin, cyclin D1 and c-myc. CONCLUSIONS: Our findings suggested that LINC01503 conferred oncogenic function in glioma and may be a new prognostic biomarker and novel therapeutic strategy for this malignancy.


Assuntos
Glioma/genética , Glioma/metabolismo , RNA Longo não Codificante/metabolismo , beta Catenina/metabolismo , Feminino , Glioma/diagnóstico , Humanos , Masculino , Pessoa de Meia-Idade , RNA Longo não Codificante/genética , RNA Longo não Codificante/isolamento & purificação , Células Tumorais Cultivadas , Regulação para Cima , Via de Sinalização Wnt/genética , beta Catenina/genética
4.
Nat Commun ; 5: 4584, 2014 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-25081579

RESUMO

Correlated electron oxide heterojunctions and their photovoltaic effect have attracted increasing attention from the viewpoints of both possible application to novel devices and basic science. In such junctions, correlated electron physics has to be taken into account in addition to conventional semiconductor modelling to explain distinctively emerging features. However, extracting novel functionalities has not been easy because it is not possible to predict their interfacial properties solely from their bulk characteristics. Here we describe a magneto-tunable photocurrent in a pn junction based on a correlated electron oxide La0.7Sr0.3MnO3 combined with a semiconducting SrTiO3 substrate. On applying an epitaxial strain, the photocurrent is enhanced threefold, which is increased 30% further by a magnetic field. Such a magneto-tunable effect is possible for only a narrow window of the correlated gap, which is itself adjusted by bandwidth and temperature. These results provide a guideline for utilization of correlated phenomena into the novel electronic devices.

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