WHEN INTERACTING ONLINE LEADS TO TAKING ACTION OFFLINE: EXAMINING THE EFFECTS OF ONLINE PERSUASION ON IS USERS’ PRO-ENVIRONMENTAL BEHAVIOURS

With the increasing attention towards the role of information systems (IS) as a vehicle to address environmental issues, IS researchers and practitioners have strived to leverage advanced Green IS innovations to persuade people to engage in environmentally responsible practices and support pro-environmental initiatives. Yet, existing research reveals that the persuasion effects of Green IS designs remain equivocal. In particular, many design characteristics advocated in Green IS research can produce bi-directional changes in IS users’ attitudes and behaviours. To address this issue, this thesis drew upon the circumplex model of social values (S.H. Schwartz, 1992) to explain when and how online persuasion designs come to affect people’s judgements on resource conservation and environmental protection. Three sets of working propositions and specific hypotheses were developed. Specifically, this research suggests that the use of an IS application can elicit different value primes and draw IS users’ attentions to different motivational functions of engaging in suggested behavioural changes. It is expected that matching online persuasion appeals with IS users’ personal value priorities can increase users’ acceptance of online behavioural suggestions. Second, it is hypothesized that the persuasion effect tends to be weakened, as the system users become aware of the valuematching design in a given IS application. Third, it is proposed that different value primes presented in an IS application can result in different unintended effects on IS users’ global pro-environmental attitudes and motivations. The hypotheses were tested in the two pilot studies and two full-scale online experiments. The study findings generally support the main predictions of the hypotheses. On the one hand, this thesis providesiii empirical evidence that IS design for online persuasion can be instrumental in influencing IS users’ judgements on a range of resource conservation practices. On the other hand, this work explains why the effectiveness of IS-enabled online persuasion attempts needs to be measured not only in terms of the intended changes in a target behavioural domain but also in terms of unintended changes in people’s general environmental orientations. Findings in this research may bring a different perspective on understanding and assessing the influence of Green IS applications on IS users’ judgements and behaviou

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.