Interleukin-6 serves as a critical factor in various cancer progression and therapy.

Interleukin-6 (IL-6), a pro-inflammatory cytokine, plays a crucial role in host immune defense and acute stress responses. Moreover, it modulates various cellular processes, including proliferation, apoptosis, angiogenesis, and differentiation. These effects are facilitated by various signaling pathways, particularly the signal transducer and activator of transcription 3 (STAT3) and Janus kinase 2 (JAK2). However, excessive IL-6 production and dysregulated signaling are associated with various cancers, promoting tumorigenesis by influencing all cancer hallmarks, such as apoptosis, survival, proliferation, angiogenesis, invasiveness, metastasis, and notably, metabolism. Emerging evidence indicates that selective inhibition of the IL-6 signaling pathway yields therapeutic benefits across diverse malignancies, such as multiple myeloma, prostate, colorectal, renal, ovarian, and lung cancers. Targeting key components of IL-6 signaling, such as IL-6Rs, gp130, STAT3, and JAK via monoclonal antibodies (mAbs) or small molecules, is a heavily researched approach in preclinical cancer studies. The purpose of this study is to offer an overview of the role of IL-6 and its signaling pathway in various cancer types. Furthermore, we discussed current preclinical and clinical studies focusing on targeting IL-6 signaling as a therapeutic strategy for various types of cancer.

Assessing the gas sensing capability of undoped and doped aluminum nitride nanotubes.

CONTEXT: CO2 and CO gas sensors are very important to recognize the insulation situation of electrical tools. ToCO explore the application of noble metal doped of aluminum nitride nanotubes for gas sensors, DFT computations according to the first principal theory were applied to study sensitivity, adsorption attributes, and electronic manner. In this investigation, platinum-doped aluminum nitride nanotubes were offered for the first time to analyze the adsorption towards CO2 and CO gases. Firm construction of platinum-doped aluminum nitride nanotubes (Pt-AlNNT) was investigated in four feasible places, and the binding energy of firm construction is 1.314 eV. Respectively, the adsorption energy between the CO2 and Pt-AlNNT systems was - 2.107 eV, while for instance of CO, the adsorption energy was - 3.258 eV. The mentioned analysis and computations are considerable for studying Pt-AlNNT as a new CO2 and CO gas sensor for electrical tools insulation. The current study revealed that the Pt-AlNNT possesses high selectivity and sensitivity towards CO2 and CO. METHODS: In this research, Pt-doped AlNNT (Pt-AlNNT) has been studied as sensing materials of CO and CO2 for the first time. The adsorption process of Pt-AlNNT has been computed and analyzed through the DFT approach. DFT computations by using B3LYP functional and 6-31 + G* basis sets have been applied in the GAMESS code for sensing attributes, which contribute to potential applications.

A state-of-art of underlying molecular mechanisms and pharmacological interventions/nanotherapeutics for cisplatin resistance in gastric cancer.

The fourth common reason of death among patients is gastric cancer (GC) and it is a dominant tumor type in Ease Asia. One of the problems in GC therapy is chemoresistance. Cisplatin (CP) is a platinum compound that causes DNA damage in reducing tumor progression and viability of cancer cells. However, due to hyperactivation of drug efflux pumps, dysregulation of genes and interactions in tumor microenvironment, tumor cells can develop resistance to CP chemotherapy. The current review focuses on the CP resistance emergence in GC cells with emphasizing on molecular pathways, pharmacological compounds for reversing chemoresistance and the role of nanostructures. Changes in cell death mechanisms such as upregulation of pro-survival autophagy can prevent CP-mediated apoptosis that results in drug resistance. Moreover, increase in metastasis via EMT induction induces CP resistance. Dysregulation of molecular pathways such as PTEN, PI3K/Akt, Nrf2 and others result in changes in CP response of GC cells. Non-coding RNAs determine CP response of GC cells and application of pharmacological compounds with activity distinct of CP can result in sensitivity in tumor cells. Due to efficacy of exosomes in transferring bioactive molecules such as RNA and DNA molecules among GC cells, exosomes can also result in CP resistance. One of the newest progresses in overcoming CP resistance in GC is application of nanoplatforms for delivery of CP in GC therapy that they can increase accumulation of CP at tumor site and by suppressing carcinogenic factors and overcoming biological barriers, they increase CP toxicity on cancer cells.