RESUMEN
The SiS+ cation is considered a potential astromolecule, yet there is limited documentation regarding its spectroscopic properties and spectral line intensities. In this paper, the potential energy curves, dipole moments, and transition dipole moments of the SiS+ cation are calculated using the icMRCI + Q method. By solving the one-dimensional Schrödinger equation for the nucleus, we have obtained spectroscopic constants for both the ground state and 11 low-lying excited states. Utilizing the vibrational transition energy levels of these 12 bound states, we calculated the partition function for the SiS+ cation over the temperature range of 300-10,000 K. Upon deriving the partition function and Einstein coefficients, we have computed the spectral line intensities for the X2Π state, the A2Σ+ state, and the X2Π â A2Σ+ transition at 300 and 3000 K for Δν = 0,1,2. At T = 300 K, the intensity of the X2Π state 1-0 band reaches its maximum, while at T = 3000 K, the intensity of the A2Σ+ state 0-0 band reaches its maximum. The spectral line intensities of the X2Π â A2Σ+ transition, on the other hand, are relatively small, with the overall intensity being smaller compared to the spectral line intensities of the X2Π and A2Σ+ states by about 10-6.
RESUMEN
For the first time, the spectroscopy and transition properties of SeCl+ are systematically reported. The potential energy curves of 22 Λ - S states and the corresponding 51 Ω states in the first and second dissociation channels of SeCl+ are calculated using the internally contracted multiconfiguration interaction and Davidson correction method. The phenomenon of avoided crossing in Ω states below 30,000 cm-1 is discussed in detail. The spectroscopy constants are obtained by fitting the potential energy curves, and also the Franck-Condon factors and radiation lifetimes of the X3Σ0+- â 21Σ0++ transition are calculated. Between X3Σ0+- and 21Σ0++, the Franck-Condon factors are large, close to 1, but the radiation lifetime is large too. According to the calculation results, it is determined that direct laser cooling of SeCl+ is considered infeasible.
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In this paper, potential energy curves of Λ-S and Ω states of SBr+ are reported for the first time, and the spectrum data of some low excited bound states are obtained. The differences in the spectrum properties of main-group molecules and SBr+ were compared and analyzed, providing a sufficient theoretical basis for the subsequent study of main-group molecules. The avoided crossing that occurs in the Ω state is analyzed, and finally it is concluded that this phenomenon mainly occurs in the energy region between 20,000 and 40,000 cm-1 that is relative to the minimum energy value. Potential transitions in the Ω state capable of achieving laser cooling of SBr+ are explored. The Franck-Condon factor, radiation lifetime, and Einstein coefficient between X3Σ0+- and b1Σ0++ are calculated. From the calculation results, we concluded that direct laser cooling of SBr+ is not feasible. What we have studied in this paper provides a theoretical basis for subsequent computational exploration of the spectrum properties of SBr+.
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Our previous studies found overexpression of Musashi2 (MSI2) conduced to the progression and chemoresistance of pancreatic cancer (PC) by negative regulation of Numb and wild type p53 (wtp53). Now, we further investigated the novel signalling involved with MSI2 in PC. We identified inositol-3-phosphate synthase 1 (ISYNA1) as a novel tumour suppressor regulated by MSI2. High MSI2 and low ISYNA1 expression were prevalently observed in 91 PC tissues. ISYNA1 expression was negatively correlated with MSI2 expression, T stage, vascular permeation and poor prognosis in PC patients. What's more, patients expressed high MSI2 and low ISYNA1 level had a significant worse prognosis. And in wtp53 Capan-2 and SW1990 cells, ISYNA1 was downregulated by p53 silencing. ISYNA1 silencing promoted cell proliferation and cell cycle by inhibiting p21 and enhanced cell migration and invasion by upregulating ZEB-1. However, MSI2 silencing upregulated ISYNA1 and p21 but downregulated ZEB-1, which can be rescued by ISYNA1 silencing. Moreover, reduction of cell migration and invasion resulting from MSI2 silencing was significantly reversed by ISYNA1 silencing. In summary, MSI2 facilitates the development of PC through a novel ISYNA1-p21/ZEB-1 pathway, which provides new gene target therapy for PC.
Asunto(s)
Carcinoma Ductal Pancreático/patología , Inhibidor p21 de las Quinasas Dependientes de la Ciclina/fisiología , Liasas Intramoleculares/fisiología , Proteínas de Neoplasias/fisiología , Neoplasias Pancreáticas/patología , Proteínas de Unión al ARN/fisiología , Transducción de Señal/fisiología , Homeobox 1 de Unión a la E-Box con Dedos de Zinc/fisiología , Adulto , Anciano , Carcinoma Ductal Pancreático/genética , Carcinoma Ductal Pancreático/mortalidad , Carcinoma Ductal Pancreático/secundario , Línea Celular Tumoral , Movimiento Celular , Inhibidor p21 de las Quinasas Dependientes de la Ciclina/biosíntesis , Inhibidor p21 de las Quinasas Dependientes de la Ciclina/genética , Progresión de la Enfermedad , Femenino , Regulación Neoplásica de la Expresión Génica , Humanos , Liasas Intramoleculares/antagonistas & inhibidores , Liasas Intramoleculares/biosíntesis , Liasas Intramoleculares/genética , Estimación de Kaplan-Meier , Neoplasias Hepáticas/secundario , Metástasis Linfática , Masculino , Persona de Mediana Edad , Invasividad Neoplásica , Proteínas de Neoplasias/antagonistas & inhibidores , Proteínas de Neoplasias/biosíntesis , Proteínas de Neoplasias/genética , Neoplasias Pancreáticas/genética , Neoplasias Pancreáticas/mortalidad , Pronóstico , Interferencia de ARN , ARN Interferente Pequeño/genética , ARN Interferente Pequeño/farmacología , Proteína p53 Supresora de Tumor/fisiología , Homeobox 1 de Unión a la E-Box con Dedos de Zinc/biosíntesis , Homeobox 1 de Unión a la E-Box con Dedos de Zinc/genéticaRESUMEN
BACKGROUND: To our knowledge, there are no studies to systematically compare the detailed clinical significance between curatively resected pancreatic head (ph) and body-tail (pbt) ductal adenocarcinoma based on the new 8th edition of AJCC staging system (8th AJCC stage) that was just applied in clinical practice in 2018. METHODS: Three hundred fifty-one patients with curatively resected pancreatic adenocarcinoma (PC) from three center hospitals were entered into this multicenter cohort study. RESULTS: Increasing tumor size (P < 0.001), T stage (T1 + T2 vs T3 + T4, P = 0.003), frequent postoperative liver metastasis (PLM) (P = 0.002) and 8th AJCC stage (IA to VI, P < 0.001; I + II vs III + IV, P = 0.002) were closely associated with the progression of pbt cancers compared with that in ph cancer patients. Moreover, tumor size≥3 cm (P = 0.012), 8th AJCC stage (III + IV) (P = 0.025) and PLM (P = 0.010) were identified as independent risk factors in pbt cancers in logistic analysis. Patients with pbt cancers had a significantly worse overall survival compared with ph cancer patients (P = 0.003). Moreover, pbt was an independent unfavorable factor in multivariate analysis (P = 0.011). In addition to lymph nodes metastasis, 8th AJCC stage, vascular invasion and PLM, increasing tumor size and advanced T stage were also closely associated with the poor prognosis in 131 cases of pbt cancer patients compared with Ph cancer patients. CONCLUSION: Pbt, as an independent unfavorable factor for the prognosis of PC patients, are much more aggressive than that in ph cancers according to 8th AJCC staging system. 8th AJCC staging system are more comprehensive and sensitive to reflect the malignant biology of pbt cancers.
Asunto(s)
Carcinoma Ductal Pancreático/mortalidad , Carcinoma Ductal Pancreático/cirugía , Estadificación de Neoplasias/métodos , Pancreatectomía/métodos , Neoplasias Pancreáticas/mortalidad , Neoplasias Pancreáticas/cirugía , Anciano , Carcinoma Ductal Pancreático/clasificación , Carcinoma Ductal Pancreático/patología , China , Estudios de Cohortes , Femenino , Estudios de Seguimiento , Humanos , Estimación de Kaplan-Meier , Neoplasias Hepáticas/secundario , Metástasis Linfática , Masculino , Persona de Mediana Edad , Neoplasias Pancreáticas/clasificación , Neoplasias Pancreáticas/patología , Factores de Riesgo , Tasa de Supervivencia , Resultado del Tratamiento , Carga TumoralRESUMEN
Self-control enables people to resist short-term temptations in the service of long-term goals. Previous exertion of self-control leads to a state of ego depletion. Three studies demonstrated that ego depletion leads to a high level of unethical behavior. These studies also hypothesized and confirmed that depleted individuals behave unethically because of low moral identity. Study 1 found that depleted participants were more likely to over-report their performance than non-depleted participants. Study 2 revealed that depletion reduced people's moral identity, which in turn increased their propensity to engage in unethical behavior. Study 3 proved that priming moral identity eliminated the effect of depletion on cheating. Findings suggest that reduced moral identity accounts for the effect of self-control depletion on unethical behavior.
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Decepción , Principios Morales , Autocontrol , Análisis y Desempeño de Tareas , Adulto , Ego , Femenino , Humanos , Masculino , Autocontrol/psicología , Test de Stroop , Adulto JovenRESUMEN
OBJECTIVE: The objective of this study is to systematically assess the clinical efficacy of hand-assisted laparoscopic surgery (HALS) and laparoscopic right colectomy (LRC). METHODS: The randomized controlled trials (RCTs) and non-RCTs were collected by searching electronic databases (Pubmed, Embase, and the Cochrane Library). The outcomes included intraoperative outcomes, postoperative outcomes, postoperative morbidity, and oncologic outcomes. Meta-analysis was performed using of RevMan 5.3 software. RESULTS: A total of five studies involving 438 patients were finally included, with 202 cases in HALS group and 236 cases in LRC group. Results of meta-analysis showed that there was no statistical difference between HALS and LRC in terms of conversion rate, length of hospital stay, reoperation rate, postoperative morbidity, and oncologic outcomes. The operative time was 6.5 min shorter in HALS group; however, it was not a clinically significant difference. Although the incision length was longer in HALS, it did not influence the postoperative recovery. CONCLUSIONS: HALS can be considered an alternative to LRC which combines the advantages of open as well as laparoscopic surgery.
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Colectomía/métodos , Enfermedades del Colon/cirugía , Laparoscópía Mano-Asistida/métodos , Laparoscopía/métodos , Complicaciones Posoperatorias/epidemiología , Colectomía/efectos adversos , Ensayos Clínicos Controlados como Asunto , Conversión a Cirugía Abierta/estadística & datos numéricos , Laparoscópía Mano-Asistida/efectos adversos , Humanos , Laparoscopía/efectos adversos , Tiempo de Internación/estadística & datos numéricos , Tempo Operativo , Periodo Perioperatorio/estadística & datos numéricos , Complicaciones Posoperatorias/etiología , Resultado del TratamientoRESUMEN
In this paper, the potential energy curves of 22 Λ-S states as well as 51 Ω states were calculated using the internally contracted multiconfiguration interaction and Davidson correction method. Through the obtained transition data, the spectroscopy data of the low excitation bound state are fitted and compared with the same main group ions. The phenomenon of avoided crossing that occurs in the Ω state is analyzed, and finally it is concluded that this phenomenon mainly occurs in the energy region between 20 000 cm-1 and 40 000 cm-1. The potential laser cooling transition cycle in the Ω state is analyzed. The Franck-Condon factor, radiative lifetime and Einstein coefficient between are calculated. In this paper, we argue that direct laser cooling of SeBr+ is not feasible. The content of our study provides a theoretical basis for subsequent calculations to explore the properties of SeBr+ spectrum.
RESUMEN
For the first time, the spectroscopy data of TeCl+ ion and the transition data between low excited states are systematically calculated. The potential energy curves of 22 Λ-S states and 51 Ω states are calculated by the internally contracted multiconfiguration interaction and Davidson correction method. By solving the one-dimensional radial Schrödinger equation, the spectroscopy data of Λ-S states and Ω states are obtained. The phenomenon of avoided crossing in Ω state is analyzed in detail, which is mainly concentrated in the region of 20000 cm-1 to 35000 cm-1. The Franck-Condon factors, Einstein coefficients and spontaneous radiative lifetimes of [Formula: see text] transitions are calculated. According to the calculation results, it is preliminarily judged that the direct laser cooling of TeCl+ ion is not feasible.
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Serine-arginine protein kinase 2 (SRPK2) is aberrantly expressed in human malignancies including colorectal cancer (CRC). However, little is known about the molecular mechanisms, and the role of SRPK2 in chemosensitivity remains unexplored in CRC. We recently showed that SRPK2 promotes pancreatic cancer progression by down-regulating Numb and p53. Therefore, we investigated the cooperation between SRPK2, Numb and p53 in the cell migration, invasion and chemosensitivity of CRC in vitro. Here, we showed that SRPK2 expression was higher in CRC tumors than in nontumor tissues. SRPK2 expression was positively associated with clinicopathological characteristics of CRC patients, including tumor differentiation, T stage, N stage and UICC stage. Additionally, SRPK2 had no association with mutant p53 (mtp53) in SW480 and SW620 cells, but negatively regulated Numb and wild-type p53 (wtp53) in response to 5-fluorouracil or cisplatin treatment in HCT116 cells. Moreover, SRPK2, Numb and p53 coimmunoprecipitated into a triple complex with or without the treatment of 5-fluorouracil in HCT116 cells, and p53 knockdown reversed the up-regulation of wtp53 induced by SRPK2 silencing with chemical agent treatment. Furthermore, overexpression of SRPK2 increased cell migration and invasion and decreased chemosensitivity to 5-fluorouracil or cisplatin in HCT116 cells. Conversely, SRPK2 silencing decreased cell migration and invasion and increased chemosensitivity to 5-fluorouracil or cisplatin, yet these effects could be reversed by p53 knockdown under chemical agent treatment. These results thus reveal a novel role of SRPK2-Numb-p53 signaling in the progression of CRC and demonstrate that SRPK2 is a potential therapeutic target for CRC clinical therapy.
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Neoplasias Colorrectales/tratamiento farmacológico , Neoplasias Colorrectales/metabolismo , Proteínas de la Membrana/metabolismo , Proteínas del Tejido Nervioso/metabolismo , Proteínas Serina-Treonina Quinasas/metabolismo , Proteína p53 Supresora de Tumor/metabolismo , Línea Celular Tumoral , Movimiento Celular/efectos de los fármacos , Movimiento Celular/fisiología , Proliferación Celular/efectos de los fármacos , Proliferación Celular/fisiología , Cisplatino/farmacología , Neoplasias Colorrectales/patología , Progresión de la Enfermedad , Femenino , Fluorouracilo/farmacología , Células HCT116 , Humanos , Masculino , Persona de Mediana Edad , Invasividad Neoplásica/genética , Invasividad Neoplásica/patología , Estadificación de Neoplasias/métodos , Transducción de Señal/efectos de los fármacos , Transducción de Señal/fisiologíaRESUMEN
An amendment to this paper has been published and can be accessed via the original article.
RESUMEN
BACKGROUND: Our previous study showed Musashi2 (MSI2) promoted chemotherapy resistance and pernicious biology of pancreatic cancer (PC) by down-regulating Numb and p53. We further explored the novel molecular mechanism involving its oncogenic role in PC development. METHODS: We investigated the potential role and mechanism of MSI2 in EGF-induced EMT in PC in vitro and vivo. RESULTS: EGF enhanced EGFR (epidermal growth factor receptor) phosphorylation, induced EMT and activated ZEB1-ERK/MAPK signaling in 2 PC cells. However, MSI2 silencing reversed EGF stimulated function, including inhibiting EGF-promoted EMT-like cell morphology and EGF-enhanced cell invasion and migration. Meanwhile, MSI2 silencing inhibited EGF-enhanced EGFR phosphorylation at tyrosine 1068 and reversed EGF-induced change of the key proteins in EMT and ZEB1-ERK/MAPK signaling (ZEB1, E-cad, ZO-1, ß-catenin, pERK and c-Myc). Additionally, MSI2 was co-stained and co-immunoprecipitated with ZEB1, pERK and c-Myc in PC cells by IF and co-IP, implying a close interaction between them. In vivo, MSI2 silencing inhibited pancreatic tumor size in situ and distant liver metastases. A close relationship of MSI2 with EMT and ZEB1-ERK/MAPK signaling were also observed in vivo and human PC samples, which coordinately promoted the poor prognosis of PC patients. CONCLUSIONS: MSI2 promotes EGF-induced EMT in PC via ZEB1-ERK/MAPK signaling.
RESUMEN
BACKGROUND: Our previous study showed that calreticulin (CRT) promoted EGF-induced epithelial-mesenchymal transition (EMT) in pancreatic cancer (PC) via Integrin/EGFR-ERK/MAPK signaling. We next investigated the novel signal pathway and molecular mechanism involving the oncogenic role of CRT in PC. METHODS: We investigated the potential role and mechanism of CRT in regulating intracellular free Ca2+ dependent acute and chronic endoplasmic reticulum stress (ERS)-induced EMT in PC in vitro and vivo. RESULTS: Thapsigargin (TG) induced acute ERS via increasing intracellular free Ca2+ in PC cells, which was reversed by CRT silencing. Additionally, CRT silencing inhibited TG-induced EMT in vitro by reversing TG-induced changes of the key proteins in EMT signaling (ZO-1, E-cadherin and Slug) and ERK/MAPK signaling (pERK). TG-promoted cell invasion and migration was also rescued by CRT silencing but enhanced by IRE1α silencing (one of the key stressors in unfolded protein response). Meanwhile, CRT was co-immunoprecipitated and co-localized with IRE1α in vitro and its silencing led to the chronic ERS via upregulating IRE1α independent of IRE1-XBP1 axis. Moreover, CRT silencing inhibited IRE1α silencing-promoted EMT, including inhibiting the activation of EMT and ERK/MAPK signaling and the promotion of cell mobility. In vivo, CRT silencing decreased subcutaneous tumor size and distant liver metastasis following with the increase of IRE1α expression. A negative relationship between CRT and IRE1α was also observed in clinical PC samples, which coordinately promoted the advanced clinical stages and poor prognosis of PC patients. CONCLUSIONS: CRT promotes EMT in PC via mediating intracellular free Ca2+ dependent TG-induced acute ERS and IRE1α-mediated chronic ERS via Slug and ERK/MAPK signaling.
Asunto(s)
Biomarcadores de Tumor/metabolismo , Calcio/metabolismo , Calreticulina/metabolismo , Estrés del Retículo Endoplásmico , Transición Epitelial-Mesenquimal , Regulación Neoplásica de la Expresión Génica , Neoplasias Pancreáticas/patología , Animales , Apoptosis , Biomarcadores de Tumor/genética , Calreticulina/genética , Proliferación Celular , Endorribonucleasas/genética , Endorribonucleasas/metabolismo , Femenino , Humanos , Masculino , Ratones , Ratones Endogámicos BALB C , Ratones Desnudos , Persona de Mediana Edad , Neoplasias Pancreáticas/genética , Neoplasias Pancreáticas/metabolismo , Pronóstico , Proteínas Serina-Treonina Quinasas/genética , Proteínas Serina-Treonina Quinasas/metabolismo , Tasa de Supervivencia , Células Tumorales Cultivadas , Proteína 1 de Unión a la X-Box/genética , Proteína 1 de Unión a la X-Box/metabolismo , Ensayos Antitumor por Modelo de XenoinjertoRESUMEN
Serine/arginine protein-specific kinase 2 (SRPK2) plays a vital role in the progression of a range of different malignancies, including pancreatic cancer. However, the mechanisms are poorly understood. Previous studies have shown that in hepatocellular carcinoma, SRPK2 knockdown leads to the upregulation of the cell fate determining protein Numb, and in pancreatic cancer cells, Numb knockdown prevents ubiquitin-mediated degradation of p53. In this study, we investigated the relationship between SRPK2, Numb and p53 in the development of pancreatic cancer with or without chemical agent treatment in vitro. SRPK2 expression was upregulated in pancreatic cancer tissues and associated with decreased overall survival in pancreatic cancer patients, indicating that expression of this protein can be used as a marker of unfavourable prognosis. Expression of SRPK2 was positively associated with tumour T stage and Union for International Cancer Control (UICC) stage, and negatively associated with Numb expression in serial tissue sections. In pancreatic cancer cells, SRPK2 downregulation or overexpression led to modulation of Numb and wild-type p53 protein expression in response to oxaliplatin treatment. Furthermore, these three endogenous proteins could be coimmunoprecipitated as a triple complex. Numb or p53 knockdown reversed the upregulation of p53 that was induced by silencing SRPK2. SRPK2 overexpression promoted cell invasion and migration, and decreased chemosensitivity of cancer cells to gemcitabine or oxaliplatin treatment. Conversely, SRPK2 silencing decreased cell invasion and migration and increased chemosensitivity; these effects were reversed by silencing p53 in oxaliplatin-treated pancreatic cancer cells. Our data suggest that SRPK2 negatively regulates p53 by downregulating Numb under chemical agent treatment. Thus, SRPK2 promotes the development and progression of pancreatic cancer in a p53-dependent manner.
Asunto(s)
Regulación Neoplásica de la Expresión Génica , Proteínas de la Membrana/biosíntesis , Proteínas de Neoplasias/fisiología , Proteínas del Tejido Nervioso/biosíntesis , Neoplasias Pancreáticas/enzimología , Proteínas Serina-Treonina Quinasas/fisiología , Proteína p53 Supresora de Tumor/biosíntesis , Anciano , Antineoplásicos/farmacología , Biomarcadores de Tumor , Línea Celular Tumoral , Movimiento Celular , Desoxicitidina/análogos & derivados , Desoxicitidina/farmacología , Progresión de la Enfermedad , Resistencia a Antineoplásicos , Femenino , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Silenciador del Gen , Humanos , Estimación de Kaplan-Meier , Neoplasias Hepáticas/secundario , Masculino , Proteínas de la Membrana/genética , Persona de Mediana Edad , Invasividad Neoplásica , Proteínas de Neoplasias/biosíntesis , Proteínas de Neoplasias/genética , Estadificación de Neoplasias , Proteínas del Tejido Nervioso/genética , Oxaliplatino/farmacología , Neoplasias Pancreáticas/mortalidad , Neoplasias Pancreáticas/patología , Proteínas Serina-Treonina Quinasas/antagonistas & inhibidores , Proteínas Serina-Treonina Quinasas/biosíntesis , Proteínas Serina-Treonina Quinasas/genética , Proteína p53 Supresora de Tumor/antagonistas & inhibidores , Proteína p53 Supresora de Tumor/genética , GemcitabinaRESUMEN
Evaluative conditioning (EC) procedures can be used to form and change attitudes toward a wide variety of objects. The current study examined the effects of a negative EC procedure on attitudes toward chocolate, and whether it influenced chocolate evaluation and consumption. Participants were randomly assigned to the experimental condition in which chocolate images were paired with negative stimuli, or the control condition in which chocolate images were randomly paired with positive stimuli (50%) and negative stimuli (50%). Explicit and implicit attitudes toward chocolate images were collected. During an ostensible taste test, chocolate evaluation and consumption were assessed. Results revealed that compared to participants in the control condition, participants in the experimental condition showed more negative explicit and implicit attitudes toward chocolate images and evaluated chocolate more negatively during the taste test. However, chocolate consumption did not differ between experimental and control conditions. These findings suggest that pairing chocolate with negative stimuli can influence attitudes toward chocolate, though behavioral effects are absent. Intervention applications of EC provide avenues for future research and practices.
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Our previous study showed that Calreticulin (CRT) promoted the development of pancreatic cancer (PC) through ERK/MAPK pathway. We next investigate whether CRT promotes EGF-induced epithelial-mesenchymal transition (EMT) in PC via Integrin/EGFR-ERK/MAPK signaling, which has not been reported yet to our knowledge. EGF simultaneously induced EMT and activated Integrin/EGFR-ERK/MAPK signaling pathway in 3 PC cells. However, CRT silencing significantly inhibited EGF function, including inhibiting EGF-induced EMT-like cell morphology, EGF-enhanced cell invasion and migration, and EGF induced the decrease of E-cadherin, ZO-1, and ß-catenin and the increase of the key proteins in Integrin/EGFR-ERK/MAPK signaling (pEGFR-tyr1173, Fibronectin, Integrinß1, c-Myc and pERK). Conversely, CRT overexpression rescued the change of EMT-related proteins induced by EGF in CRT silencing PC cells. Additionally, CRT was co-stained with pEGFR1173 (with EGF), Fibronectin and Integrinß1 by IF under confocal microscopy and was co-immunoprecipitated with Fibronectin, Integrinß1 and c-Myc in both PC cells, all of which indicating a close interaction of CRT with Integrin/EGFR-ERK/MAPK signaling pathway in PC. In vivo, CRT silencing inhibited subcutaneous tumor growth and liver metastasis of pancreatic tumor. A positive relationship of CRT with Fibronectin, Integrinß1, c-Myc and pERK and a negative association of CRT with E-cad was also observed in vivo and clinical samples. Meanwhile, overexpression of the above proteins was closely associated with multiple aggressive clinicopathological characteristics and the poor prognosis of PC patients. CRT promotes EGF-induced EMT in PC cells via Integrin/EGFR-ERK/MAPK signaling pathway, which would be a promising therapy target for PC.
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Calreticulina/metabolismo , Carcinoma Ductal Pancreático/metabolismo , Factor de Crecimiento Epidérmico/metabolismo , Integrinas/metabolismo , Sistema de Señalización de MAP Quinasas , Neoplasias Pancreáticas/metabolismo , Animales , Carcinoma Ductal Pancreático/enzimología , Carcinoma Ductal Pancreático/patología , Línea Celular Tumoral , Transición Epitelial-Mesenquimal , Xenoinjertos , Humanos , Ratones , Ratones Endogámicos BALB C , Ratones Desnudos , Neoplasias Pancreáticas/enzimología , Neoplasias Pancreáticas/patología , TransfecciónRESUMEN
Ego depletion has been found to moderate the effect of implicit preferences on food consumption, such that implicit preferences predict consumption only under a depleted state. The present study tested how trait impulsivity impacts the effect of implicit preferences on food consumption in a depleted condition. Trait impulsivity was measured by means of self-report and a stop signal task. Results showed that both self-reported impulsivity and behavioral impulsivity moderated the 'depletion and then eating according to implicit preferences' effect, albeit in different ways. Participants high in self-reported impulsivity and low in behavioral impulsivity were more vulnerable to the effect of depletion on eating. The implications of these results for extant theories are discussed. Future research is needed to verify whether or not trait impulsivity is associated with vulnerability to depletion across different self-control domains.