Lung adenocarcinoma (LUAD) is the commonest subtype of non-small cell lung cancer (NSCLC). 1,2 Despite significant progress achieved in clinical and experimental ontology, the prognosis of LUAD still presents a gloomy prospective. 3,4 Early diagnosis is important for the successful treatment of LUAD, and however, patients with LUAD usually are diagnosed at advanced stage or with metastasis. 5 Therefore, the identification of novel diagnosis and therapeutic biomarkers for LUAD patients is in great urgency.Over the past decade, with development of whole-genome sequencing technology, particular attention has been paid on the exploding class of transcripts of long non-coding RNAs (lncRNAs), arbitrarily defined according to a length over 200 nucleotides. 6,7 Once considered as transcriptional noise, lncRNAs are now revealed by steadily growing lists to play authentic biological roles. Many lncRNAs are identified to share common characteristics

Lung cancer remains the leading cause of cancer deaths. Non-small cell lung cancer (NSCLC) is the most frequent subtype of lung cancer. Surgery, radiation, chemotherapy, immunotherapy, or molecularly targeted therapy is used to treat NSCLC. Nevertheless, many patients who accept surgery likely develop distant metastases or local recurrence. In recent years, targeted treatments and immunotherapy have achieved improvement at a breakneck pace. Therapy must be customized for each patient based on the specific medical condition, as well as other variables. It is critical to have an accurate NSCLC sub-classification for tailored treatment, according to the latest World Health Organization standards.

Background/Aim: High mobility group box 1 protein (HMGB1) is functionally dynamic and pleiotropic molecule, it has the potential to promote both cell survival and death by regulating multiple signaling pathways, including inflammation and apoptosis. This study aimed at investigating the role of silencing HMGB1 on tumor cells apoptosis and pro-inflammatory proteins expression in hepatocellular HepG2 cancer cells. Methods: HepG2 cells was transfected with si-RNA HMGB1, and the effect on pro-apoptotic proteins expressions like Bax, Bcl2, and pro-inflammatory cytokines like, p65-NFκB, and Cyclooxygenase-2 (Cox2) was assessed using western blot, and also cells apoptosis and proliferation was assessed using annexin V FITC and Calcien AM expression in flow cytometry and fluorescence. Results: HMGB1 silencing was found significantly increase tumor cells viability with significant decrease of pro-apoptotic proteins, also antiapoptotic protein Bcl2 was significantly up-regulated, which suggests a possible role in restricting apoptosis. Furthermore, HMGB1 knocked down found to inhibit Stat3 phosphorylation and significantly affect NFkB p65/Cox2 expression which suggests a link between HMGB1 and Stat3 activation. Our results revealed that HMGB1 knocked down may suppress cells apoptosis and enhance HepG2 cells viability via NFkB/Cox2 and Stat3. © 2018 BioFactors, 44(6):570-576, 2018 Keywords: HMGB1 knock down; NFκB; STAT3, Cox2Abbreviations: Cox2, Cyclooxygenase-2; HMGB1, High mobility group box 1 protein; NAC, N-acetyl-L-cysteine; NFκB, nuclear factor kappa B; Stat3, Signal transducer and activator of transcription 3

Non-small-cell lung cancer takes up the majority of lung carcinoma-caused deaths. It is reported that targeting PD-1/PD-L1, a well-known immune evasion checkpoint, can eradicate tumor. Checkpoint inhibitors, such as monoclonal antibodies, are actively employed in cancer treatment. Thus, this review aimed to assess the therapeutic and toxic effects of PD-1/PD-L1 inhibitors in treatment of NSCLC. So far, 6 monoclonal antibodies blocking PD-1/PD-L1 interaction are identified and used in clinical trials and randomized controlled trials for NSCLC therapy. These antibody-based therapies for NSCLC were collected by using search engine PubMed, and articles about the assessment of adverse events were collected by using Google search. Route of administration and dosage are critical parameters for efficient immunotherapy. Although antibodies can improve overall survival and are expected to be target-specific, they can cause systemic adverse effects in the host. Targeting certain biomarkers can limit the toxicity of adverse effects of the antibody-mediated therapy. Clinical experts with knowledge of adverse effects (AEs) of checkpoint inhibitors can help manage and reduce mortalities associated with antibody-based therapy of NSCLC.