La-related protein 1 (LARP1) is a conserved RNA-binding protein and is known to regulate 5'-terminal oligopyrimidine tract (TOP) mRNA translation. Dysregulated LARP1 has been reported to be related to the development of several cancers. However, the exact function and mechanism of LARP1 in non-small cell lung cancer (NSCLC) is largely unknown. In the present study, we found that the mRNA levels of LARP1 were increased in NSCLC cells compared to those in normal control cells. Knockdown of LARP1 inhibited cell proliferation, migration and invasion in NSCLC cells and tumourigenicity in H520 cells. Both in vitro and in vivo analyses confirmed that STAT3 signalling was inactivated by the knockdown of LARP1. Moreover, LARP1 was identified as a direct target of miR-374a. Overexpression of miR-374a attenuated the promotor effects of LARP1 by inhibiting proliferation, metastasis and STAT3 signalling. Clinically, LARP1 was markedly overexpressed in NSCLC tissues, and upregulated LARP1 was correlated with tumour progression and poor survival. The expression of miR-374a was negatively correlated with the expression of LARP1 in NSCLC tissues. Furthermore, we found that XIST functioned as a competing endogenous RNA to suppress miR-374a, which regulated its downstream target LARP1. In summary, we suggest that the dysfunction of the XIST/miR-374a/LARP1 axis contributes to NSCLC and may serve as a promising therapeutic strategy for treatment.
SummaryAutophagy can mediate antiviral immunity. However, it remains unknown whether autophagy regulates the immune response of dendritic cells (DCs) to influenza A (H1N1) pdm09 infection. In this study, we found that infection with the H1N1 virus induced DC autophagy in an endocytosis-dependent manner. Compared with autophagy-deficient Beclin-1 +/À mice, we found that bone-marrow-derived DCs from wild-type mice (WT BMDCs) presented a more mature phenotype on H1N1 infection. Wildtype BMDCs secreted higher levels of interleukin-6 (IL-6), tumour necrosis factor-a ( Our data indicate that autophagy is important in the regulation of the DC immune response to H1N1 infection, thereby extending our understanding of host immune responses to the virus.
Background: The development of paclitaxel-resistance led to the tumor relapse and treatment failure of non-small cell lung cancer. Shikonin has been demonstrated to show anti-cancer activity in many cancer types. The present study aimed to investigate the anti-cancer activity of shikonin in paclitaxel-resistant non-small cell lung cancer treatment. Methods: MTT, clonogenic assay, apoptotic cell death analysis, western blot, qRT-PCR, gene knockdown and overexpression, xenograft experiment, immunohistochemistry were performed. Results: Shikonin decreased paclitaxel-resistant NSCLC cell viability and inhibited the growth of xenograft tumor. Shikonin induced apoptotic cell death of paclitaxel-resistant NSCLC cell lines and suppressed the level of NEAT1 and Akt signaling of paclitaxel-resistant NSCLC cell lines and xenograft tumors. Either low dose or high dose of shikonin considerably suppressed the cell growth and induced the cell apoptotic death in NEAT1 knockdown A549/ PTX cells, and p-Akt expression was decreased. Conclusions: Shikonin could be a promising candidate for paclitaxel-resistant NSCLC treatment.
What Is Known and Objective: The aim of this study was to evaluate the pharmacokinetics of paclitaxel in cancer patients with hypoalbuminemia following paclitaxelcontaining chemotherapy and to provide a reference for the prevention of adverse events (AEs) after paclitaxel administration.Methods: Peripheral blood was collected from cancer patients treated with paclitaxel.The plasma concentration of paclitaxel was determined by ultra-high performance liquid chromatography after 24 ± 8 h of chemotherapy, and individual paclitaxel time above a threshold concentration of 0.05 μmol/L (T c>0.05 ) was calculated using the population pharmacokinetic model. Haematological and non-haematological toxicities were monitored after chemotherapy, and the correlation between different chemotherapy toxicities and T c>0.05 was evaluated using the Prism software.Results and Discussion: The enrolled patients were divided into the hypoalbuminemia group and normal albumin level group. The mean T c>0.05 values in the normal albumin level and hypoalbuminemia groups were 36.89 and 24.93 h, respectively (P < 0.001). The risk of myelosuppression was positively correlated with T c>0.05 . Due to the lower T c>0.05 , the incidences of immediate AEs such as gastrointestinal reactions and rashes were higher in the hypoalbuminemia group than in the normal albumin level group, and the incidences of delayed AEs such as myelosuppression and neurotoxicity were lower in the hypoalbuminemia group.What Is New and Conclusions: Plasma albumin level has a conclusive effect on T c>0.05 , which can predict the potential clinical toxicity of paclitaxel. The study provides a theoretical basis for administration of paclitaxel.
Rationale:The morbidity and mortality of small cell lung cancer (SCLC), an uncommon malignancy of the lung, remain high. Radiofrequency ablation (RFA) creates heat to destroy cancer cells and is usually used to treat non-SCLC, but not SCLC.Patient concerns:An 85-year-old male presented with a 2-month history of a productive cough with white phlegm and a 2-day history of hemoptysis. Chest computed tomography revealed a mass in the right lower lobe.Diagnoses:An excision biopsy of the mass showed SCLC.Interventions:We treated the tumor with RFA.Outcomes:At the 2-year follow-up examination, the efficacy of the RFA was evaluated as a partial response.Lessons:RFA can improve the prognosis of SCLC and should be considered for its treatment.
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