This study investigates the impact of financial inclusion on environmental sustainability in 178 emerging and developing countries from 1996 to 2022. Employing a composite index derived through Principal Component Analysis (PCA) as a measure of financial inclusion and covering four aspects (access, depth, efficiency, stability), our analysis reveals negative outcomes. The findings indicate that enhancing financial inclusion is associated with a notable increase in CO2 per capita emissions as well as in Total Greenhouse Gas emissions. We demonstrate that controlling corruption improves environmental quality, yet this measure alone is insufficient to fully mitigate the impact of financial inclusion, as indicated by our moderation analysis. The same analysis, however, shows that fostering globalization through trade openness is an efficient tool to alleviate the positive effect of financial inclusion on the quality of the environment. The study employs various policies targeting the control of development levels, energy consumption, natural resource utilization, industry, and urban population dynamics to contextualize the influence of financial inclusion on environmental sustainability. Through econometric methods and a comprehensive examination of the specified time frame, our results provide insights into the complex interplay between financial inclusion and environmental outcomes in diverse socio-economic contexts. The research contributes to the discourse on sustainable development by highlighting the potential of certain factors as a catalyst for environmental improvement. Understanding these dynamics is crucial for policymakers, as it underlines the trade-off between integrating inclusive financial strategies and achieving environmentally sustainable development trajectories in emerging and developing nations. Moreover, shedding light on the underlying mechanisms, such as trade-offs, fills a significant gap in the literature.

Although docetaxel treatment yields a high survival rate for prostate cancer (PCa), resistance eventually develops in many patients. Understanding the underlying mechanisms of docetaxel resistance is essential for improving treatment strategies. Cytokines, which play a role in cell signaling and immune responses, have been implicated in drug resistance mechanisms. The study revealed that interleukin-8 (IL-8) was consistently overexpressed in both docetaxel-resistant PCa cell lines. Thus, the expression levels of cytokines released from docetaxel-sensitive (PC-3- and DU-145) and resistant (PC-3/R-DU-145/R) PCa cells were compared. IL-8 was found to be commonly expressed in resistant cell lines. This finding led to the hypothesis that IL-8 could play a key role in mediating PCa cell resistance to docetaxel. IL-8 siRNA treatment increased docetaxel sensitivity in both resistant cells. To demonstrate the mechanism of IL-8-related resistance, MDR1 expression was evaluated. After IL-8 siRNA treatment MDR1 expression was reduced in both resistant cells suggesting that IL-8 regulates the docetaxel resistance of PCa cells via modulation of multidrug resistance 1 (MDR1). By expanding the knowledge of the cytokines and their effect mechanisms, novel approaches can be developed for the treatment of docetaxel-resistant prostate cancer. Further investigations into the role of IL-8 in docetaxel resistance could offer valuable insights into the development of effective treatment strategies for PCa patients.