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1.
Pathol Res Pract ; : 152850, 2020 Feb 05.
Artigo em Inglês | MEDLINE | ID: mdl-32046874

RESUMO

BACKGROUND: Hepatocellular carcinoma (HCC) is an aggressive malignant tumor with poor prognosis that is characterized by high rates of postoperative recurrence and mortality. Understanding the molecular mechanism of this malignancy is of great significance for the development of new and effective strategies for the treatment of hepatocellular carcinoma. Thyroid hormone receptor-interacting protein 6 (TRIP6), also known as zyxin-related protein-1 or ZRP-1, is an adaptor protein that belongs to the zyxin family of LIM proteins. Recent studies showed that TRIP6 is involved in carcinogenesis. But the functional role of TRIP6 in HCC has not been reported to date. METHODS: TRIP6 expression level in HCC cell lines and normal cell line was measured by qPCR. The roles of TRIP6 on HCC cell proliferation, colony formation, and invasion were examined by MTT assay, colony formation assay, and transwell invasion assay, respectively. The effect of TRIP6 on the overall survival of HCC patients was further analyzed. ChIP assay and western blot were performed to validate whether FOXC1 was involved in the regulation of TRIP6 expression. RESULTS: Western blot and immunohistochemical analyses showed that TRIP6 expression was up-regulated in HCC tissues compared with adjacent non-tumor tissues. Kaplan-Meier survival analysis indicated that upregulation of TRIP6 was dramatically associated with poor overall survival. TRIP6 knockdown significantly inhibited cell migration, invasion, and proliferation, and its effect on cell proliferation was mediated by the modulation of cell cycle progression. FOXC1 also played a vital role in TRIP6 regulation. TRIP6 mediated the FOXC1-regulated proliferation, invasion, and migration in vitro and tumor growth in vivo. CONCLUSIONS: These results suggest that TRIP6 may contribute to the invasiveness and metastasis of HCC cells, and provide new insight into the crucial role of TRIP6 in tumorigenesis and cancer progression.

2.
Nat Commun ; 11(1): 618, 2020 Jan 30.
Artigo em Inglês | MEDLINE | ID: mdl-32001715

RESUMO

The coupling between spin, charge, and lattice degrees of freedom plays an important role in a wide range of fundamental phenomena. Monolayer semiconducting transitional metal dichalcogenides have emerged as an outstanding platform for studying these coupling effects. Here, we report the observation of multiple valley phonons - phonons with momentum vectors pointing to the corners of the hexagonal Brillouin zone - and the resulting exciton complexes in the monolayer semiconductor WSe2. We find that these valley phonons lead to efficient intervalley scattering of quasi particles in both exciton formation and relaxation. This leads to a series of photoluminescence peaks as valley phonon replicas of dark trions. Using identified valley phonons, we also uncover an intervalley exciton near charge neutrality. Our work not only identifies a number of previously unknown 2D excitonic species, but also shows that monolayer WSe2 is a prime candidate for studying interactions between spin, pseudospin, and zone-edge phonons.

3.
J Pineal Res ; : e12640, 2020 Feb 17.
Artigo em Inglês | MEDLINE | ID: mdl-32064655

RESUMO

Melatonin is a well-studied neurohormone oscillating in a 24-hour cycle in vertebrates. Phytomelatonin is widespread in plant kingdom, but it remains elusive whether this newly-characterized putative hormone underlies the regulation by daily rhythms. Here, we report phytomelatonin signaling, as reflected by changes in endogenous concentrations of phytomelatonin and expression of genes associated with biosynthesis of phytomelatonin (AtSNAT1, AtCOMT1 and AtASMT) and its receptor (AtPMTR1), shows 24-hour oscillations in Arabidopsis. The variation of reactive oxygen species (ROS) production and scavenging and expression of ROS-related genes significantly decrease in pmtr1 and snat and increase in PMTR1-OE seedlings, indicating the rhythmicity in phytomelatonin signaling is required for maintenance of ROS dynamics. Additionally, the ROS signaling feedback influences the expression of AtSNAT1, AtCOMT1, AtASMT, and AtPMTR1, suggesting the phytomelatonin and ROS signaling are coordinately interrelated. The pmtr1 mutant plants lose diurnal stomatal closure, with stomata remaining open during daytime as well as nighttime and mutants showing more water loss and drought sensitivity when compared with the wild type Col-0 plants. Taken together, our results suggest that PMTR1-regulated ROS signaling peaks in the afternoon and may transmit the darkness signals to trigger stomatal closure, which might be essential for high water-use efficiency and drought tolerance.

4.
Plant Cell Environ ; 2020 Feb 03.
Artigo em Inglês | MEDLINE | ID: mdl-32012302

RESUMO

The circadian pacemaker in plants is a hierarchical multioscillator system that directs and maintains a 24-hr oscillation required for organism homeostasis and environmental fitness. Molecular clockwork within individual tissues and organs acts cell autonomously, showing differences in circadian expression of core oscillators and their target genes; there are functional dominance and coupling in the complex regulatory network. However, molecular characteristics of organ-specific clocks are still unknown. Here, we showed the detached shoot and root possess dynamic circadian protein-protein interactions between clock core components, periodicity in organs exhibits a difference. The period length difference between shoot and root was not remarkable in prr7-3 and prr7-3 prr9-1 mutants. In addition, the phase transition curve indicated that shoot and root clock respond differently to the resetting cues of ambient temperature. PRR9 and PRR7 compensate circadian period between 22°C and 28°C in shoot, not in root. The circadian rhythms of PRR9 or PRR7 transcript accumulation showed no difference at 22°C and 28°C in shoot, but differences were observed in root. In summary, our results reveal the specificity of dynamic circadian protein-protein interactions in organ-autonomous clocks and the critical roles of PRR9 and PRR7 in mechanisms regulating temperature compensation in aerial shoot system.

5.
Sensors (Basel) ; 20(4)2020 Feb 12.
Artigo em Inglês | MEDLINE | ID: mdl-32059442

RESUMO

To create an intelligent surface region of interests (ROI) 3D quantitative inspection strategy a reality in the continuous casting (CC) production line, an improved 3D laser image scanning system (3D-LDS) was established based on binocular imaging and deep-learning techniques. In 3D-LDS, firstly, to meet the requirements of the industrial application, the CCD laser image scanning method was optimized in high-temperature experiments and secondly, we proposed a novel region proposal method based on 3D ROI initial depth location for effectively suppressing redundant candidate bounding boxes generated by pseudo-defects in a real-time inspection process. Thirdly, a novel two-step defects inspection strategy was presented by devising a fusion deep CNN model which combined fully connected networks (for defects classification/recognition) and fully convolutional networks (for defects delineation). The 3D-LDS' dichotomous inspection method of defects classification and delineation processes are helpful in understanding and addressing challenges for defects inspection in CC product surfaces. The applicability of the presented methods is mainly tied to the surface quality inspection for slab, strip and billet products.

6.
J Immunother Cancer ; 8(1)2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-32051287

RESUMO

BACKGROUND: Pancreatic cancer (PC) is a common malignancy of the digestive system and is characterized by poor prognosis and early metastasis. Tumor immune escape plays an important role in PC progression. Programmed death 1 (PD1) blockade therapy is a promising treatment for patients with PC, but is yet to achieve significant clinical effects so far. Interferon gamma (IFN-γ) is a soluble dimeric cytokine that is closely associated with tumor immune surveillance and cytotoxicity. IFN-γ suppresses a variety of tumor-derived cytokines in PC, such as CXCL8. In the present study, we investigated the therapeutic efficacy of combined anti-PD1 and IFN-γ treatment in PC. METHODS: BxPC-3 and Panc-1 human PC cell lines were used to construct a murine PC model. Blood samples (n=44) and surgical resection specimens (n=36) from human patients with PC were also collected. χ2 test, two-tailed unpaired t-test or Kaplan-Meier survival analysis was used to calculate p values. RESULTS: PD1/PD-L1 signaling was overexpressed in PC tumor-bearing mice. Anti-PD1 prevented tumor growth if initiated early after tumor inoculation; however, delayed anti-PD1 treatment showed limited benefit. Murine PC model had a preferential expansion of CXCR2+CD68+ macrophages, and these cells showed an immunosuppressive nature (M2 polarization). PC tumors overexpressed CXCL8 and tumor-derived CXCL8 deficiency prohibited the trafficking of CXCR2+CD68+ macrophages. IFN-γ suppressed the expression of tumor-derived CXCL8, and combined with IFN-γ treatment, delayed anti-PD1 treatment showed significant antitumor effects. Thus, we conclude that murine CXCR2+CD68+ macrophages traffic to PC tumors by tumor-derived CXCL8 and mediate local immunosuppression, which limits the efficacy of PD1 blockade therapy. IFN-γ suppresses tumor-derived CXCL8 and inhibits the tumor trafficking of CXCR2+CD68+ macrophages by blocking the CXCL8-CXCR2 axis to enhance anti-PD1 efficacy. Human PC also produces high levels of CXCL8. Patients with PC present elevated CXCR2 expression on peripheral and tumor-infiltrating CD68+ macrophages, which are associated with advanced tumor stage and poor prognosis. CONCLUSION: Our findings suggest that IFN-γ is a translatable, therapeutic option to improve the efficacy of PD1 blockade therapy by preventing trafficking of CXCR2+CD68+ macrophages via blocking the CXCL8-CXCR2 axis.

7.
Nano Lett ; 2020 Feb 17.
Artigo em Inglês | MEDLINE | ID: mdl-32031382

RESUMO

We have synthesized unique colloidal nanoplatelets of the two-dimensional (2D) van der Waals ferromagnet CrI3 and have characterized these nanoplatelets structurally, magnetically, and by magnetic circular dichroism spectroscopy. The CrI3 nanoplatelets have lateral dimensions of ∼25 nm and thicknesses of only ∼4 nm, corresponding to just a few CrI3 monolayers. Magnetic and magneto-optical measurements demonstrate robust 2D ferromagnetic ordering with Curie temperatures similar to bulk CrI3, despite their small size. These data also show magnetization steps akin to those observed in micron-sized few-layer 2D sheets associated with concerted spin-reversal of individual CrI3 layers within few-layer van der Waals stacks. Similar data have also been obtained for CrBr3 and anion-alloyed Cr(I1-xBrx)3 nanoplatelets. These results represent the first example of lateral nanostructures of 2D van der Waals ferromagnets of any composition. The demonstration of robust ferromagnetism at nanometer lateral dimensions opens new doors for miniaturization in spintronics devices based on van der Waals ferromagnets.

8.
J Cell Physiol ; 2020 Jan 29.
Artigo em Inglês | MEDLINE | ID: mdl-31994191

RESUMO

Development of the acquired resistance is one major obstacle during chemotherapy for cancer patients. Exosomes mediate intercellular communication and cause environmental changes in tumor progression by transmitting active molecules. In this study, the role of long noncoding RNA H19 within exosomes is elucidated in terms of regulating doxorubicin (DOX) resistance of breast cancer. As a result, increased H19 expression was observed in DOX-resistant breast cancer cells in comparison with the corresponding parental cells. Suppression of H19 significantly lowered DOX resistance by decreasing cell viability, lowering colony-forming ability, and inducing apoptosis. Moreover, extracellular H19 could be moved to sensitive cells via being incorporated into exosomes. Treating sensitive cells with exosomes from resistant cells increased the chemoresistance of DOX, while downregulation of H19 in sensitive cells abated this effect. Taken together, H19 could be delivered by exosomes to sensitive cells, leading to the dissemination of DOX resistance. Our finding highlights the potential of exosomal H19 as a molecular target to reduce DOX resistance.

9.
Nat Nanotechnol ; 2020 Jan 27.
Artigo em Inglês | MEDLINE | ID: mdl-31988503

RESUMO

Magnetic proximity effects are integral to manipulating spintronic1,2, superconducting3,4, excitonic5 and topological phenomena6-8 in heterostructures. These effects are highly sensitive to the interfacial electronic properties, such as electron wavefunction overlap and band alignment. The recent emergence of magnetic two-dimensional materials opens new possibilities for exploring proximity effects in van der Waals heterostructures9-12. In particular, atomically thin CrI3 exhibits layered antiferromagnetism, in which adjacent ferromagnetic monolayers are antiferromagnetically coupled9. Here we report a layer-resolved magnetic proximity effect in heterostructures formed by monolayer WSe2 and bi/trilayer CrI3. By controlling the individual layer magnetization in CrI3 with a magnetic field, we show that the spin-dependent charge transfer between WSe2 and CrI3 is dominated by the interfacial CrI3 layer, while the proximity exchange field is highly sensitive to the layered magnetic structure as a whole. In combination with reflective magnetic circular dichroism measurements, these properties allow the use of monolayer WSe2 as a spatially sensitive magnetic sensor to map out layered antiferromagnetic domain structures at zero magnetic field as well as antiferromagnetic/ferromagnetic domains at finite magnetic fields. Our work reveals a way to control proximity effects and probe interfacial magnetic order via van der Waals engineering13.

10.
Nat Nanotechnol ; 2020 Jan 06.
Artigo em Inglês | MEDLINE | ID: mdl-31907441

RESUMO

The coupling between spin and charge degrees of freedom in a crystal gives rise to magneto-optical effects with applications in the sensitive detection of local magnetic order, optical modulation and data storage. In two-dimensional magnets these effects manifest themselves in the large magneto-optical Kerr effect1,2, spontaneous helical light emission3,4 from ferromagnetic (FM) monolayers and electric-field induced Kerr rotation5-7 and giant second-order non-reciprocal optical effects8 in antiferromagnetic (AFM) bilayers. Here we demonstrate the tuning of inelastically scattered light through symmetry control in atomically thin chromium triiodide (CrI3). In monolayers, we found an extraordinarily large magneto-optical Raman effect from an A1g phonon mode due to the emergence of FM order. The linearly polarized, inelastically scattered light rotates by ~40°, more than two orders of magnitude larger than the rotation from the magneto-optical Kerr effect under the same experimental conditions. In CrI3 bilayers, the same phonon mode becomes Davydov-split into two modes of opposite parity, which exhibit divergent selection rules that depend on inversion symmetry and the underlying magnetic order. We demonstrate the magneto-electrical control over these selection rules by activating or suppressing Raman activity for the odd-parity phonon mode and the magneto-optical rotation of scattered light from the even-parity phonon mode. Our work underlines the unique opportunities provided by two-dimensional magnets to control the combined time-reversal and inversion symmetries to manipulate Raman optical selection rules and for exploring emergent magneto-optical effects and spin-phonon coupled physics.

11.
Sensors (Basel) ; 19(23)2019 Nov 28.
Artigo em Inglês | MEDLINE | ID: mdl-31795216

RESUMO

Power amplifier (PA) nonlinearity is typically unique at the radio frequency (RF) front-end for particular emitters. It can play a crucial role in the application of specific emitter identification (SEI). In this paper, under the Multi-Input Multi-Output (MIMO) multipath communication scenario, two data-aided approaches are proposed to identify multi-antenna emitters using PA nonlinearity. Built upon a memoryless polynomial model, the first approach formulates a linear least square (LLS) problem and presents the closed-form solution of nonlinear coefficients in a MIMO system by means of singular value decomposition (SVD) operation. Another alternative approach estimates nonlinear coefficients of each individual PA through nonlinear least square (NLS) solved by the regularized Gauss-Newton iterative scheme. Moreover, there are some practical discussions of our proposed approaches about the mismatch of the order of PA model and the rank-deficient condition. Finally, the average misclassification rate is derived based on the minimum error probability (MEP) criterion, and the proposed approaches are validated to be effective through extensively numerical simulations.

12.
J Exp Clin Cancer Res ; 38(1): 497, 2019 Dec 18.
Artigo em Inglês | MEDLINE | ID: mdl-31852504

RESUMO

BACKGROUND: The survival of pancreatic cancer patients remains poor. However, the underlying molecular mechanism and new therapeutic target of pancreatic cancer are still needed to be found. Many studies have shown that the IGF2 mRNA-binding protein 2 (IGF2BP2) plays oncogenic roles in cancers. However, the clinical significance, role and molecular mechanisms of IGF2BP2 in pancreatic cancer remain unclear. METHODS: The expression of IGF2BP2 and miR-141 was detected in pancreatic cancer, and clinical significances were analyzed by statistical analysis. The function of IGF2BP2 and miR-141 was determined in vitro and in vivo, and the underlying mechanism was investigated. The gene copy number variation (CNV) of IGF2BP2 was analyzed based on The Cancer Genome Atlas (TCGA) dataset. microRNAs (miRNAs) regulating IGF2BP2 were predicted by online tools and confirmed by experiments. RESULTS: IGF2BP2 is overexpressed in pancreatic cancer tissues compared with control tissues. Upregulation of IGF2BP2 predicts shorter overall survival (OS) in pancreatic cancer patients by statistical analysis. IGF2BP2 overexpression is partially due to genomic amplification. Bioinformatics analyses and validation experiments showed that IGF2BP2 is a direct target of miR-141. A negative correlation between IGF2BP2 mRNA expression and the expression of miR-141 was observed in pancreatic cancer tissues and more importantly, reexpression of miR-141 rescued the oncogenic role of IGF2BP2. Moreover, upregulating IGF2BP2 expression promotes pancreatic cancer cell growth by activating the PI3K/Akt signaling pathway in vitro and in vivo. CONCLUSIONS: We comprehensively reveal the oncogenic role of IGF2BP2 in pancreatic cancer carcinogenesis and confirm that genomic amplification and the silencing of miR-141 contribute to its activation. Our findings highlight that IGF2BP2 may be a promising molecular target for the treatment of pancreatic cancer.

13.
Opt Express ; 27(22): 31783-31789, 2019 Oct 28.
Artigo em Inglês | MEDLINE | ID: mdl-31684403

RESUMO

Two compact mid-infrared microchip lasers at 2717 and 2740 nm have been demonstrated using a Er:Y2O3 ceramic as laser gain medium with thickness of 800 µm, for the first time to our knowledge. Under a 976-nm diode laser pumping, the 2717 nm microchip laser with linewidth of about 0.16 nm is achieved with a maximum output power of 234.8 mW and slope efficiency of about 10.9%. The laser beam quality expressed by M2 factor is measured to be about 1.23 and 1.45 in x and y directions. A single wavelength at 2740 nm with linewidth of about 0.15 nm is also achieved with maximum output power of 102 mW and slope efficiency of about 4.9%. Beam quality of the 2740 nm laser is found to be about 1.15 and 1.26 in x and y directions. Using a mechanical chopper to modulate the pump laser for thermal mitigation, the maximum output powers can be further improved to 312 mW for 2717 nm laser and 145 mW for 2740 m laser at higher pump powers. Such a mid-infrared microchip laser source with very compact size could be have great potential in various eye-safety-related applications.

14.
Chemotherapy ; 64(3): 146-154, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31715603

RESUMO

OBJECTIVE: Colorectal cancer (CRC) remains a major cause of cancer-related death worldwide. Proteasome 26S subunit ATPase 2 (PSMC2) plays vital roles in regulating cell cycle and transcription and has been confirmed to be a gene potentially associated with some human tumors. However, the expression correlation and molecular mechanism of PSMC2 in CRC are still unclear. This study aimed to investigate the role of PSMC2 in malignant behaviors in CRC. METHODS: The high protein levels of PSMC2 in CRC samples were identified by tissue microarray analysis. Lentivirus was used to silence PSMC2 in HCT116 and RKO cells; MTT and colony formation assay were performed to determine cell proliferation. Wound healing and Transwell assay were used to detect cell migration and invasion. Flow cytometry assay was applied to detect cell cycle and apoptosis. RESULT: The results showed that, among the 96 CRC patients, the expression of PSMC2 was a positive correlation with the clinicopathological features of the patients with CRC. Furthermore, the low PSMC2 expression group showed a higher survival rate than the high PSMC2 expression group. The expression levels of PSMC2 in cancer tissue were dramatically upregulated compared with adjacent normal tissues. In vitro, shPSMC2 was designed to inhibit the expression of PSMC2 in CRC cells. Compared with shCtrl, silencing of PSMC2 significantly suppressed cell proliferation, decreased single cell colony formation, enhanced apoptosis, and accelerated G2 phase and/or S phase arrest. CONCLUSION: Survival analysis indicated that high expression of PSMC2 in the CRC samples was associated with poorer survival rate than low expression of PSMC2, while the anti-tumor effect of PSMC2 silencing was also confirmed at the cellular level in vitro. Our results suggested that PSMC2 potentially worked as a regulator for CRC, and the silencing of PSMC2 may be a therapeutic strategy for CRC.


Assuntos
ATPases Associadas a Diversas Atividades Celulares/metabolismo , Apoptose , Proliferação de Células , Neoplasias Colorretais/patologia , Complexo de Endopeptidases do Proteassoma/metabolismo , Interferência de RNA , ATPases Associadas a Diversas Atividades Celulares/antagonistas & inibidores , ATPases Associadas a Diversas Atividades Celulares/genética , Idoso , Linhagem Celular Tumoral , Movimento Celular , Neoplasias Colorretais/metabolismo , Neoplasias Colorretais/mortalidade , Feminino , Humanos , Estimativa de Kaplan-Meier , Masculino , Prognóstico , Complexo de Endopeptidases do Proteassoma/genética , RNA Interferente Pequeno/metabolismo , Pontos de Checagem da Fase S do Ciclo Celular
15.
Plant Cell Environ ; 2019 Nov 14.
Artigo em Inglês | MEDLINE | ID: mdl-31724182

RESUMO

In plants, the spatiotemporal expression of circadian oscillators provides adaptive advantages in diverse species. However, the molecular basis of circadian clock in soybean is not known. In this study, we used soybean hairy roots expression system to monitor endogenous circadian rhythms and the sensitivity of circadian clock to environmental stimuli. We discovered in experiments with constant light and temperature conditions that the promoters of clock genes GmLCLb2 and GmPRR9b1 drive a self-sustained, robust oscillation of about 24-h in soybean hairy roots. Moreover, we demonstrate that circadian clock is entrainable by ambient light/dark or temperature cycles. Specifically, we show that light and cold temperature pulses can induce phase shifts of circadian rhythm, and we found that the magnitude and direction of phase responses depends on the specific time of these two zeitgeber stimuli. We obtained a quadruple mutant lacking the soybean gene GmLCLa1, LCLa2, LCLb1, and LCLb2 using CRISPR, and found that loss-of-function of these four GmLCL orthologs leads to an extreme short-period circadian rhythm and late-flowering phenotype in transgenic soybean. Our study establishes that the morning-phased GmLCLs genes act constitutively to maintain circadian rhythmicity and demonstrates that their absence delays the transition from vegetative growth to reproductive development.

16.
Science ; 366(6468): 983-987, 2019 11 22.
Artigo em Inglês | MEDLINE | ID: mdl-31753996

RESUMO

Controlling the crystal structure is a powerful approach for manipulating the fundamental properties of solids. In van der Waals materials, this control can be achieved by modifying the stacking order through rotation and translation between the layers. Here, we observed stacking-dependent interlayer magnetism in the two-dimensional (2D) magnetic semiconductor chromium tribromide (CrBr3), which was enabled by the successful growth of its monolayer and bilayer through molecular beam epitaxy. Using in situ spin-polarized scanning tunneling microscopy and spectroscopy, we directly correlate the atomic lattice structure with the observed magnetic order. Although the individual monolayer CrBr3 is ferromagnetic, the interlayer coupling in bilayer depends on the stacking order and can be either ferromagnetic or antiferromagnetic. Our observations pave the way for manipulating 2D magnetism with layer twist angle control.

17.
World J Gastroenterol ; 25(42): 6311-6321, 2019 Nov 14.
Artigo em Inglês | MEDLINE | ID: mdl-31754292

RESUMO

BACKGROUND: Studies have reported that microRNA-30c (miR-30c) has vital functions in the development and progression of multiple cancers. AIM: To investigate the clinical significance and role of miR-30c in pancreatic cancer. METHODS: MiR-30c and twinfilin 1 (TWF1) expression levels were analyzed in Gene Expression Omnibus datasets and validated in human pancreatic cancer by quantitative real-time polymerase chain reaction (RT-qPCR). The effects of miR-30c on pancreatic cancer cell growth, apoptosis, and cell cycle were evaluated by CCK-8 and flow cytometry assays. Furthermore, the in vivo effects were investigated using a subcutaneous xenograft experiment. Target gene prediction software and luciferase reporter assays were used to identify TWF1 as a direct target of miR-30c. RESULTS: The expression of miR-30c was significantly decreased in pancreatic cancer tissues and associated with survival. Gain- and loss-of-function assays showed that miR-30c suppressed pancreatic cancer cell proliferation in vitro and in vivo. RT-qPCR, Western blot, and luciferase reporter assays showed that miR-30c directly targeted TWF1. The expression level of miR-30c was negatively correlated with TWF1 expression in pancreatic cancer tissues. Furthermore, the effects of ectopic miR-30c were rescued by TWF1 overexpression. CONCLUSION: Our results identified the role of the miR-30c/TWF1 axis in pancreatic cancer progression and demonstrated that miR-30c might serve as a prognostic biomarker and therapeutic target for pancreatic cancer.

18.
Int J Biol Sci ; 15(12): 2750-2762, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31754344

RESUMO

The role of the novel oncogene, mitochondrial transcription termination factor (MTERFD1), in human colorectal cancer (CRC) is unclear. Here, we report the role MTERFD1 in CRC. We conducted plasmid construction and transfection analyses, cell proliferation assays, apoptosis detection assays, ELISA, western blotting, and qRT-PCR using cell culture applications. MTERFD1 was upregulated in human and chemically induced mouse CRC tissues. In vitro functional assays showed that MTERFD1 overexpression promoted human CRC cell proliferation, whereas knockdown of endogenous MTERFD1 significantly enhanced apoptosis in these cells. MTERFD1 expression was positively linked to irradiation resistance in CRC cells. Furthermore, interleukin (IL)-6 and IL-11 were identified as the effector molecules of MTERFD1 in its oncogenic role and irradiation resistance in CRC cells. Our results demonstrated that MTERFD1 played an oncogenic role in CRC development and enhanced irradiation resistance by regulating IL-6 and IL-11 in CRC cells. MTERFD1 may serve as a potential prognostic and therapeutic marker for radiotherapy in CRC.

19.
Nat Mater ; 18(12): 1298-1302, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31659293

RESUMO

The physical properties of two-dimensional van der Waals crystals can be sensitive to interlayer coupling. For two-dimensional magnets1-3, theory suggests that interlayer exchange coupling is strongly dependent on layer separation while the stacking arrangement can even change the sign of the interlayer magnetic exchange, thus drastically modifying the ground state4-10. Here, we demonstrate pressure tuning of magnetic order in the two-dimensional magnet CrI3. We probe the magnetic states using tunnelling8,11-13 and scanning magnetic circular dichroism microscopy measurements2. We find that interlayer magnetic coupling can be more than doubled by hydrostatic pressure. In bilayer CrI3, pressure induces a transition from layered antiferromagnetic to ferromagnetic phase. In trilayer CrI3, pressure can create coexisting domains of three phases, one ferromagnetic and two antiferromagnetic. The observed changes in magnetic order can be explained by changes in the stacking arrangement. Such coupling between stacking order and magnetism provides ample opportunities for designer magnetic phases and functionalities.

20.
Oncol Lett ; 18(4): 4160-4166, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31579419

RESUMO

Colorectal cancer (CRC) is the third leading cause of cancer-associated mortality worldwide. Ginsenoside Rh1 (Rh1) is a traditional medicine monomer with antitumor activity; however, the effects of Rh1 in CRC remain to be determined. In the present study, SW620 cells were treated with different concentrations of Rh1. Cell Counting Kit-8, wound healing and Transwell assays were performed to measure cell viability and proliferation, migration and invasion, respectively. Subsequently, the mRNA expression levels of matrix metallopeptidase (MMP)1, MMP3 and tissue inhibitor of metalloproteinases 3 (TIMP3) were detected by reverse transcription-quantitative PCR analysis. In addition, the protein expression levels of MMP1, MMP3, TIMP3, and total or phosphorylated (p-)ERK1/2, P38, JNK were detected by western blotting. Furthermore, tumor growth was examined in a nude mouse xenograft model. The results of the present study indicated that Rh1 was not toxic to CRC cells at various concentrations (0, 50 or 100 µM) and treatment durations (24 or 48 h). However, cell proliferation was suppressed by Rh1 in a dose-dependent manner. Rh1 (100 µM) significantly inhibited cell migration and invasion in vitro. Additionally, Rh1 suppressed the mRNA and protein expression of MMP1 and MMP3, and promoted TIMP3 expression. Rh1 decreased the ratios of p-P38/P38, p-ERK1/2/ERK1-2 and p-JNK/JNK in vitro and in vivo, which suggested that Rh1 inactivated the mitogen-activated protein kinase (MAPK) signaling pathway. Notably, Rh1 markedly decreased tumor volume and weight in vivo. In conclusion, the present study demonstrated that Rh1 inhibited the proliferation, migration and invasion of CRC cells in vitro and tumor growth in vivo. This inhibition was at least partially due to the inhibition of MMP1 and MMP3 expression, the increase in TIMP3 expression level and the MAPK signaling pathway inactivation. Therefore, Rh1 may effectively inhibit the development of CRC as an anticancer drug, and may have a supporting effect during CRC treatment.

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