Highlights The disruption of the host immune system is the characteristic of the outbreak of COVID-19. Identifying the regulating mechanism of virus behavior will help design antiviral vaccine candidates. SARS-CoV-2 vaccines is critical to reduce morbidity and mortality.

A global pandemic has erupted as a result of the new brand coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This pandemic has been consociated with widespread mortality worldwide. The antiviral immune response is an imperative factor in confronting the recent coronavirus disease 2019 (COVID-19) infections. Meantime, cytokines recognize as crucial components in guiding the appropriate immune pathways in the restraining and eradication of the virus. Moreover, SARS-CoV-2 can induce uncontrolled inflammatory responses characterized by hyper-inflammatory cytokine production, which causes cytokine storm and acute respiratory distress syndrome (ARDS). As excessive inflammatory responses are contributed to the severe stage of the COVID-19 disease, therefore, the pro-inflammatory cytokines are regarded as the Achilles heel during COVID-19 infection. Among these cytokines, interleukin (IL-) 1 family cytokines (IL-1, IL-18, IL-33, IL-36, IL-37, and IL-38) appear to have a strong inflammatory role in severe COVID-19. Hence, understanding the underlying inflammatory mechanism of these cytokines during infection is critical for reducing the symptoms and severity of the disease. Here, the possible mechanisms and pathways involved in inflammatory immune responses are discussed.

Sepsis is a complex disease that begins with an infectious disorder and causes excessive immune responses. Curcumin is considered as an active component of turmeric that can improve the condition in sepsis due to its anti‐inflammatory and antioxidant properties. PubMed, Embase, Google Scholar, Web of Science, and Scopus databases were searched. Searching was not limited to a specific publication period. Only English‐language original articles, which had examined the effect of curcumin on sepsis, were included. At first, 1,098 articles were totally found, and 209 articles were selected after excluding duplicated data; 46 articles were remained due to the curcumin effects on sepsis. These included 23 in vitro studies and 23 animal studies. Our results showed that curcumin and various analogs of curcumin can have an inhibitory effect on sepsis‐induced complications. Curcumin has the ability to inhibit the inflammatory, oxidative coagulation factors, and regulation of immune responses in sepsis. Despite the promising evidence of the therapeutic effects of curcumin on the sepsis complication, further studies seem necessary to investigate its effect and possible mechanisms of action in human studies.

Sepsis is a severe reaction and an excessive immune response to infection, which can lead to organ dysfunction and death.

Lung cancer (LC) is the second common cancer for both women and men all over the world. Unfortunately, the number of LC deaths is increasing rapidly each year so early diagnosis of LC can be lifesaving. MicroRNAs are involved in multiple processes, such as cell differentiation, transcription, inflammation, proliferation, cell signaling, and apoptosis. In LC, microRNAs function as tumor suppressors (TS) or oncogenes depending on the targets. Changes in microRNAs expression level are related to tumor initiation, progression, and metastasis. MicroRNAs can regulate gene expression and thus affect the activity status of different signaling pathways including AKT, JAK-STAT, MAPK, TGF-β, WNT, and ERK signaling pathways. Positive or negative effects on drug resistance of LC are directly affected by microRNAs and their target genes. MicroRNAs can be beneficial in combination therapy with other drugs and chemotherapeutic agents for LC. K E Y W O R D S drug resistance, lung cancer, microRNA, signaling pathways, tumor suppressor How to cite this article: Asghariazar V, Sakhinia E, Mansoori B, Mohammadi A, Baradaran B. Tumor suppressor microRNAs in lung cancer: An insight to signaling pathways and drug resistance.