The promising field of organic electronics has ushered in a new era of biosensing technology, thus offering a promising frontier for applications in both medical diagnostics and environmental monitoring. This review paper provides a comprehensive overview of organic electronics’ remarkable progress and potential in biosensing applications. It explores the multifaceted aspects of organic materials and devices, thereby highlighting their unique advantages, such as flexibility, biocompatibility, and low-cost fabrication. The paper delves into the diverse range of biosensors enabled by organic electronics, including electrochemical, optical, piezoelectric, and thermal sensors, thus showcasing their versatility in detecting biomolecules, pathogens, and environmental pollutants. Furthermore, integrating organic biosensors into wearable devices and the Internet of Things (IoT) ecosystem is discussed, wherein they offer real-time, remote, and personalized monitoring solutions. The review also addresses the current challenges and future prospects of organic biosensing, thus emphasizing the potential for breakthroughs in personalized medicine, environmental sustainability, and the advancement of human health and well-being.

Niclosamide (Nic), an FDA-approved anthelmintic drug, is reported to have anti-cancer efficacy and is being assessed in clinical trials for various solid tumors. Based on its ability to target multiple signaling pathways, in the present study, we evaluated the therapeutic efficacy of Nic on pancreatic cancer (PC) in vitro. We observed an anti-cancerous effect of this drug as shown by the G0/G1 phase cell cycle arrest, inhibition of PC cell viability, colony formation, and migration. Our results revealed the involvement of mitochondrial stress and mTORC1-dependent autophagy as the predominant players of Nic-induced PC cell death. Significant reduction of Nic-induced reactive oxygen species (ROS) and cell death in the presence of a selective autophagy inhibitor spautin-1 demonstrated autophagy as a major contributor to Nic-mediated cell death. Mechanistically, Nic inhibited the interaction between BCL2 and Beclin-1 that supported the crosstalk of autophagy and apoptosis. Further, Nic treatment resulted in Gsk3β inactivation by phosphorylating its Ser-9 residue leading to upregulation of Sufu and Gli3, thereby negatively impacting hedgehog signaling and cell survival. Nic induced autophagic cell death, and p-Gsk3b mediated Sufu/Gli3 cascade was further confirmed by Gsk3β activator, LY-294002, by rescuing inactivation of Hh signaling upon Nic treatment. These results suggested the involvement of a non-canonical mechanism of Hh signaling, where p-Gsk3β acts as a negative regulator of Hh/Gli1 cascade and a positive regulator of autophagy-mediated cell death. Overall, this study established the therapeutic efficacy of Nic for PC by targeting p-Gsk3β mediated non-canonical Hh signaling and promoting mTORC1-dependent autophagy and cell death.

The authors would like to make a correction to their published paper