The current study is the first attempt to examine the association between the Dark Triad of personality (i.e., Machiavellianism, narcissism, and psychopathy) and corruption through a mediator—belief in good luck. Based on Ajzen's theory of planned behavior, we assumed that individuals with Dark Triad would be more likely to engage in corruption as a result of belief in good luck. In Study 1, a set of hypothetical scenarios was used to assess the bribe-offering intention and the corresponding belief in good luck. Results indicated that while the Dark Triad of personality positively predicted bribe-offering intention, it was mediated by the belief in good luck in gain-seeking. In Study 2, we presented participants with some hypothetical scenarios of bribe-taking and the corresponding belief in good luck. Findings revealed that the Dark Triad of personality was positively related to bribe-taking intention; the relationship between narcissism and bribe-taking intention, and that between psychopathy and bribe-taking intention was mediated by the belief in good luck in penalty-avoidance. However, this belief in good luck did not mediate the relationship between Machiavellianism and bribe-taking intention. These results hold while controlling for demographic variables, dispositional optimism, and self-efficacy. Taken together, this study extended previous research by providing evidence that belief in good luck may be one of the reasons explaining why people with Dark Triad are more likely to engage in corruption regardless of the potential outcomes. Theoretical and practical implications were discussed.
The present study attempts to explore the effect of awe on environmentalism and the mediating role of social dominance orientation in generating this effect. In Study 1, a series of questionnaires were used to investigate the correlation among trait awe, social dominance orientation, and ecological behavior. Results demonstrated that, while trait awe was positively correlated with ecological behavior, it was partially mediated by social dominance orientation. In follow-up studies, two priming experiments were conducted to test the causal relationship and the psychological mechanisms between awe and environmentalism. Results revealed that inductions of awe (relative to various control states) decreased participants’ social dominance orientation, which in turn partially enhanced their willingness to make personal sacrifices for the environment (Study 2), and intentions to engage in pro-environmental behavior (Study 3). This study not only corroborates the critical role of awe in promoting environmentalism, but also highlights the importance of social dominance orientation in explaining why awe increases environmentalism. Implications and future directions were also discussed.
Protein arginine methyltransferases (PRMT) catalyze protein arginine methylation and play an important role in many biological processes. Aberrant PRMT expression in tumor cells has been documented in several common cancer types; however, its precise contribution to hepatocellular carcinoma (HCC) cell invasion and metastasis is not fully understood. In this study, we identified a new oncogene, PRMT9, whose overexpression strongly promotes HCC invasion and metastasis. PRMT9 expression was detected more frequently in HCC tissues than in adjacent noncancerous tissues. PRMT9 overexpression was significantly correlated with hepatitis B virus antigen (HBsAg) status, vascular invasion, poor tumor differentiation and advanced TNM stage. Patients with higher PRMT9 expression had a shorter survival time and higher recurrence rate. PRMT9 expression was an independent and significant risk factor for survival after curative resection. Functional studies demonstrated that PRMT9 increased HCC cell invasion and lung metastasis. Knocking down PRMT9 with short hairpin RNA (shRNA) inhibited HCC cell invasion. Further investigations found that PRMT9 increased cell migration and invasion through epithelial‐mesenchymal transition (EMT) by regulating Snail expression via activation of the PI3K/Akt/GSK‐3β/Snail signaling pathway. In clinical HCC samples, PRMT9 expression was positively associated with Snail expression and was negatively associated with E‐cadherin expression. In conclusion, our study demonstrated that PRMT9 is an oncogene that plays an important role in HCC invasion and metastasis through EMT by regulating Snail expression via activation of the PI3K/Akt/GSK‐3β/Snail signaling pathway. Thus, PRMT9 may serve as a candidate prognostic biomarker and a potential therapeutic target.
Chemokine ligand 18 (CCL18) has been associated with hepatocellular carcinoma (HCC) metastasis. Here, we demonstrated a novel mechanism through which CCL18 enhances cell migration, invasion, and epithelial-mesenchymal transition (EMT) in HCC. (1) Using immunohistochemistry, we analyzed the expression of PITPNM3, a molecule that correlated with CCL18 signaling, in 149 HCC tissue specimens. The results showed that PITPNM3 expression is highly associated with tumor metastasis and differentiation; (2) in vitro experiments showed that CCL18 enhances cell migration, invasion, and EMT in PITPNM3((+)) HCC cells but not in PITPNM3((-)) cells. Silencing of PITPNM3 by short interfering RNA (siRNA) inhibited the induction of cell migration, invasion, and EMT by CCL18; (3) Cell migration, invasion, and EMT induced by CCL18 accompanied with the phosphorylation of IKK and IKBα as well as p65 nuclear translocation in PITPNM3((+)) HCC cells, but not in the cells that PITPNM3 is silenced with siRNA, implying that the activation of NF-κB signaling is involved in the action of CCL18/PITPNM3. These results suggest that CCL18 enhances HCC cell migration, invasion, and EMT through the expression of PITPNM3 and the activation of the NF-κB signaling pathway.
Awe is an intense emotional response to perceptually vast stimuli that dramatically transcend one’s ordinary reference frame and provoke a need to adjust the current mental structures. Dispositional awe reflects individual differences in the tendency to experience awe. The current study aims to examine the effect of dispositional awe on subjective well-being, with a focus on confirming the mediating role of meaning in life and materialism. A sample of 563 Chinese adults completed measures of dispositional awe, meaning in life, materialism, and subjective well-being. Correlation analysis revealed that dispositional awe, meaning in life, and materialism were all significantly correlated with subjective well-being. Structural equation modeling showed significant paths from dispositional awe to subjective well-being through both meaning in life and materialism. Bootstrap analysis also indicated that meaning in life and materialism mediated the relationship between dispositional awe and subjective well-being. These findings not only corroborate the critical role of dispositional awe in promoting subjective well-being, but also shed some light on why people high in dispositional awe are happier than those low in dispositional awe. Limitations and directions for future research were also discussed.
Increasing evidence suggests that PRMT5, a protein arginine methyltransferase, has roles in cell growth regulation and cancer development. However, the role of PRMT5 in hepatocellular carcinoma (HCC) progression remains unclear. Here, we showed that PRMT5 expression was frequently upregulated in HCC tissues, and its expression was inversely correlated with overall survival in HCC patients. PRMT5 knockdown markedly inhibited in vitro HCC proliferation and in vivo tumorigenesis. We revealed that the mechanism of PRMT5‐induced proliferation was partially mediated by BTG downregulation, leading to cell cycle arrest during the G1 phase in HCC cells. Ectopic BTG2 overexpression decreased HCC growth, caused cell cycle arrest at the G1 phase, and downregulated Cyclin D1 and Cyclin E1 protein expression. Furthermore, we found that PRMT5‐induced ERK phosphorylation regulated BTG2 expression in HCC cells, whereas pretreatment with a selective ERK1/2 inhibitor (PD184352) significantly reversed the effect of PRMT5 on BTG2 expression. Our results indicated that PRMT5 promotes HCC proliferation by downregulating BTG2 expression via the ERK pathway.
AbsractBackgroundTumor metastasis is the major reason for poor prognosis of hepatocellular carcinoma (HCC) patients after hepatic resection. SMYD3 has been demonstrated to promote liver tumor metastasis in mice. However, the detailed molecular mechanism is still largely unknown.MethodsThe effect of SMYD3 on invasiveness and metastasis of HCC was analyzed by immunohistochemistry, migration assay, invasion assay, wound healing assay and in vivo lung metastasis assay. Mass spectrometry analysis was conducted using proteins pulled down by H3K4me3 antibody in SMYD3-overexpressing cells. Luciferase reporter, chromatin immunoprecipitation, Electrophoretic mobility shift assay were used to measure the regulation of SLUG transcription by SMYD3-ANKHD1. In addition, the role of SMYD3-ANKHD1 in determining clinical outcomes for HCC patients was investigated by immunohistochemistry in 243 HCC tissues.ResultsSMYD3 was an independent prognostic factor of HCC and promoted migration and invasion of human HCC cells. ANKHD1 was identified by mass spectrometry as a co-regulator with SMYD3. ANKHD1 interacted with H3K4me3 when cells were overexpressing SMYD3. The pro-migratory and pro-invasive effects of SMYD3 were attenuated when ANKHD1 was knocked down by siRNA. Furthermore, we found that SMYD3 bound and activated the SLUG gene promoter in a manner associated with elevating H3K4me3, H3K9Ac and H3K14Ac. Knockdown of ANKHD1 could attenuate the SMYD3-dependent activation of Slug expression. We further detected the expression of SMYD3 and ANKHD1 in 243 HCC patients and found that patients with positive coexpression of SMYD3 and ANKHD1 (SMYD3+ANKHD1+) had the shortest overall and recurrence-free survival.ConclusionOur findings provide a novel molecular mechanism for the SMYD3-regulated HCC migration and metastasis, and indicates that SMYD3-ANKHD1 may be a potential target for treating HCC.Electronic supplementary materialThe online version of this article (10.1186/s13046-018-1011-0) contains supplementary material, which is available to authorized users.
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