The mediating effect of innovation on the relationship between corporate reputation and performance in U.S. firms

In recent years, corporate reputation has gained the attention of many scholars in the strategic management and related fields. There is a general consensus that higher corporate reputation is positively related to firm success or performance. However, the link is not always straightforward; as a result, it calls for researchers to dedicate their efforts to investigate the causes and effects of firm reputation and how it is related to performance. In this doctoral dissertation, innovation is suggested as a mediating variable in this relationship. Innovation is a critical factor for firm success and survival. Highly reputed firms are in a more advantageous position to attract critical resources for innovation such as human and financial capital. These firms face constant pressure from external stakeholders, e.g. the general public, or customers, to achieve and remain at high levels of innovativeness. As a result, firms are in constant search, internally or externally, for new technologies expanding their knowledge base. Consequently, these firms engage in firms acquisitions. In the dissertation, the author assesses the effects of domestic versus international acquisitions as well as related versus unrelated acquisitions on the level of innovativeness and performance. Building upon an established measure of firm-level degree of internationalization (DOI), the dissertation proposes a more detailed and enhanced measure for the firm's DOI. It is modeled as an interaction effect between corporate reputation and resources for innovation. More specifically, firms with higher levels of internationalization will have access to resources for innovation, i.e. human and financial capital, at a global scale. Additionally, the distance between firms and higher education institutions, i.e. universities, is considered as another interaction effect for the human capital attraction. The dissertation is built on two theoretical frameworks, the resource-based view of the firm and institutional theory. It studies 211 U.S. firms using a longitudinal panel data structure from 2006 to 2012. It utilizes a linear dynamic panel data estimation methodology for its hypotheses analyses. Results confirm the hypotheses proposed in the study.

Workplace Discrimination Climate and Team Effectiveness: The Mediating Role of Collective Value Congruence, Team Cohesion, and Collective Affective Commitment

This study explored the relationship between workplace discrimination climate on team effectiveness through three serial mediators: collective value congruence, team cohesion, and collective affective commitment. As more individuals of marginalized groups diversify the workforce and as more organizations move toward team-based work (Cannon-Bowers & Bowers, 2010), it is imperative to understand how employees perceive their organization’s discriminatory climate as well as its effect on teams. An archival dataset consisting of 6,824 respondents was used, resulting in 332 work teams with five or more members in each. The data were collected as part of an employee climate survey administered in 2011 throughout the United States’ Department of Defense. The results revealed that the indirect effect through M1 (collective value congruence) and M2 (team cohesion) best accounted for the relationship between workplace discrimination climate (X) and team effectiveness (Y). Meaning, on average, teams that reported a greater climate for workplace discrimination also reported less collective value congruence with their organization (a1 = -1.07, p < .001). With less shared perceptions of value congruence, there is less team cohesion (d21 = .45, p < .001), and with less team cohesion there is less team effectiveness (b2 = .57, p < .001). In addition, because of theoretical overlap, this study makes the case for studying workplace discrimination under the broader construct of workplace aggression within the I/O psychology literature. Exploratory and confirmatory factor analysis found that workplace discrimination based on five types of marginalized groups: race/ethnicity, gender, religion, age, and disability was best explained by a three-factor model, including: career obstruction based on age and disability bias (CO), verbal aggression based on multiple types of bias (VA), and differential treatment based on racial/ethnic bias (DT). There was initial support to claim that workplace discrimination items covary not only based on type, but also based on form (i.e., nonviolent aggressive behaviors). Therefore, the form of workplace discrimination is just as important as the type when studying climate perceptions and team-level effects. Theoretical and organizational implications are also discussed.

Characterization of ALDH1A1 as a novel tumorigenic target mediating TAZ-induced lung tumorigenesis and stem cell phenotypes

Recent studies suggest that lung cancer stem cells (CSCs) may play major roles in lung cancer development, metastasis and drug resistance. Therefore, identification of lung CSC drivers may provide promising targets for lung cancer. TAZ (transcriptional co-activator with PDZ-binding motif) is a transcriptional co-activator and key downstream effector of the Hippo pathway, which plays critical roles in various biological processes. TAZ has been shown to be overexpressed in non-small cell lung cancer (NSCLC) and involved in tumorigenicity of lung epithelial cells. However, whether TAZ is a driver for lung CSCs and tumor formation in vivo is unknown. In addition, the molecular mechanism underlying TAZ-induced lung tumorigenesis remains to be determined. In this study, we provided evidence that constitutively active TAZ (TAZ-S89A) is a driver for lung tumorigenesis in vivo in mice and formation of lung CSC. Oncogenes upregulated in TAZ-overexpressing cells were identified with further validation. The most dramatically activated gene, Aldh1a1 (Aldehyde dehydrogenase 1 family member a1), a well-established CSC marker, showed that TAZ induces Aldh1a1 transcription by activating its promoter activity through interaction with the transcription factor TEA domain (TEAD) family member. Most significantly, inhibition of ALDH1A1 with its inhibitor A37 or CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) gene knockout in lung cancer cells suppressed lung tumorigenic and CSC phenotypes in vitro, and tumor formation in mice in vivo. In conclusion, this study identified TAZ as a novel inducer of lung CSCs and the first transcriptional activator of the stem cell marker ALDH1A1. Most significantly, we identified ALDH1A1 as a critical meditator of TAZ-induced tumorigenic and CSC phenotypes in lung cancer. Our studies provided preclinical data for targeting of TAZ-TEAD-ALDH1A1 signaling to inhibit CSC-induced lung tumorigenesis and drug resistance in the future.