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We focus on political marketing and conduct a systematic literature review of journal articles exploring political marketing on social media. The systematic literature review delineates the current state of political social media marketing literature. It spans six databases and comprises sixty-six journal articles published between 2011 and 2020. We identify and categorize the variables studied in the literature and develop an integrative framework that links these variables. We describe the research themes that exist in the literature. The review demonstrates that the field is growing. However, the literature is fragmented, along with being predominantly based in the US context. Conceptual and theoretical shortcomings also exist. Moreover, the literature ignores pertinent contemporary topics such as co-creation, influencer marketing, and political advertising on social media. Nevertheless, a nascent domain with growing practical significance, political social media marketing provides various exciting avenues for further research, which we outline in this study.

Appendices: Appendix 1 see Table 7. Appendix 2: You are tasked with evaluating ‘Experience WA’, a smart tourism app, while participating in a tourism experience in Western Australia. Your holiday is coming. You intend to take a five-day long trip to Perth, Western Australia. You come across ‘Experience WA’, a smart tourism app that can augment your tourism experience in Perth. ‘Experience WA’ gives you location-based information on your surroundings and can be used to plan your vacation in Perth, look up events nearby, find nearby tourism attractions, and share your holiday plans with your friends. You can use ‘Experience WA’ to search for information and plan your trip in Perth. ‘Experience WA’ can be found at the following links: Google Play Store. Apple App Store. Copyright © The Author(s) 2022. The paper identifies and analyses customers’ motives to co-create when interacting with smart services by integrating the self-determination theory with coordination mechanisms. The study also examines the how and to what extent value co-creation impacts on word-of-mouth and customer-based brand equity. An online questionnaire was employed for empirically validating the research model. The relationships were examined using partial least square path modelling. The findings show that intrinsic and extrinsic motives are significant antecedents of value co-creation. The coordination mechanisms namely, relating and knowing also significantly influence customers’ involvement in the value co-creation process. Results also show that value co-creation mediates the relationship between customers motives (intrinsic and extrinsic) to co-create and consequences. Findings of this study adds to the human–computer interaction literature by strengthening the nomological network of value co-creation when interacting with smart services by proposing a novel model integrating both the antecedents and outcomes of value co-creation. By recognizing how this practice could be motivated, service providers can bolster customer-firm interactions and enable favourable firm level consequences. Open Access funding enabled and organized by CAUL and its Member Institutions.

Most cancer cells rely on aerobic glycolysis to support uncontrolled proliferation and evade apoptosis. However, pancreatic cancer cells switch to glutamine metabolism to survive under hypoxic conditions. Activation of the Wnt/β-catenin pathway induces aerobic glycolysis by activating enzymes required for glucose metabolism and regulating the expression of glutamate transporter and glutamine synthetase. The results demonstrate that riluzole inhibits pancreatic cancer cell growth and has no effect on human pancreatic normal ductal epithelial cells. RNA-seq experiments identified the involvement of Wnt and metabolic pathways by riluzole. Inhibition of Wnt-β-catenin/TCF-LEF pathway by riluzole suppresses the expression of PDK, MCT1, cMyc, AXIN, and CyclinD1. Riluzole inhibits glucose transporter 2 expression, glucose uptake, lactate dehydrogenase A expression, and NAD + level. Furthermore, riluzole inhibits glutamate release and glutathione levels, and elevates reactive oxygen species. Riluzole disrupts mitochondrial homeostasis by inhibiting Bcl-2 and upregulating Bax expression, resulting in a drop of mitochondrial membrane potential. Finally, riluzole inhibits pancreatic cancer growth in KPC (Pdx1-Cre, LSL-Trp53R172H, and LSL-KrasG12D) mice. In conclusion, riluzole can inhibit pancreatic cancer growth by regulating glucose and glutamine metabolisms and can be used to treat pancreatic cancer.