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Background Interferon gamma (IFNγ) plays an important role in the development of chronic lung diseases via the production of inflammatory mediators, although the exact mechanism remains unclear. The present study aimed at investigating the potential mechanisms by which IFNγ induced over-production of interleukins through the interaction between carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) and phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) pathway. Methods IFN-γ induced over-production of interleukin (IL) 6 and IL8, and RNA expression of CEACAM1 and its subtypes or PI3K and its subtypes in human bronchial epithelial cells (HBE). The production of IL6 and IL8 or cell proliferation and movement were also evaluated in cellCEACAM1− or cellCEACAM1+ after the induction of IFN-γ. Roles of PI3K subtype proteins, e.g. PI3Kp110α/δ, Akt, p110α/γ/δ/β/mTOR, PI3Kp110α/δ/β, PI3Kp110δ, or pan-PI3K in IFN-γ-induced CEACAM1 subtype alterations were furthermore validated using those proteins of PI3K subtypes. Results CEACAM1, especially CEACAM1-S isoforms, was significantly up-regulated in HBE cells after treatment with IFN-γ. CEACAM1 played roles in expression of IL-6 and IL-8, and facilitated cellular proliferation and migration. IFN-γ up-regulated the expression of CEACAM1 in airway epithelial cells, especially CEACAM1-S isoforms, promoting cellular proliferation, migration, and the production of inflammatory factors. PI3K (p110δ)/Akt/mTOR pathway was involved in the process of IFN-γ-upregulated CEACAM1, especially CEACAM1-S. On the other hand, CEACAM1 could promote the activation of PI3K/Akt/mTOR pathway. Conclusion IFN-γ could induce inflammatory responses, cellular growth and proliferation through the interaction of CEACAM1 (especially CEACAM1-S isoforms) and PI3K(p110δ)/Akt/mTOR in airway epithelial cells, which might be new alternative of future therapies against epithelial transition from inflammation to cancer. Electronic supplementary material The online version of this article (10.1186/s12967-019-1894-3) contains supplementary material, which is available to authorized users.

Background Lung cancer is the leading cause of cancer-related morbidity and mortality worldwide. Patients with chronic respiratory diseases, such as chronic obstructive pulmonary disease (COPD), are exposed to a higher risk of developing lung cancer. Chronic inflammation may play an important role in the lung carcinogenesis among those patients. The present study aimed at identifying candidate biomarker predicting lung cancer risk among patients with chronic respiratory diseases. Methods We applied clinical bioinformatics tools to analyze different gene profile datasets with a special focus on screening the potential biomarker during chronic inflammation-lung cancer transition. Then we adopted an in vitro model based on LPS-challenged A549 cells to validate the biomarker through RNA-sequencing, quantitative real time polymerase chain reaction, and western blot analysis. Results Bioinformatics analyses of the 16 enrolled GSE datasets from Gene Expression Omnibus online database showed myocyte enhancer factor 2D (MEF2D) level significantly increased in COPD patients coexisting non-small-cell lung carcinoma (NSCLC). Inflammation challenge increased MEF2D expression in NSCLC cell line A549, associated with the severity of inflammation. Extracellular signal-regulated protein kinase inhibition could reverse the up-regulation of MEF2D in inflammation-activated A549. MEF2D played a critical role in NSCLC cell bio-behaviors, including proliferation, differentiation, and movement. Conclusions Inflammatory conditions led to increased MEF2D expression, which might further contribute to the development of lung cancer through influencing cancer microenvironment and cell bio-behaviors. MEF2D might be a potential biomarker during chronic inflammation-lung cancer transition, predicting the risk of lung cancer among patients with chronic respiratory diseases. Electronic supplementary material The online version of this article (doi:10.1186/s12967-017-1168-x) contains supplementary material, which is available to authorized users.

In the conventional analysis of complex diseases, the control and case samples are assumed to be of great purity. However, due to the heterogeneity of disease samples, many disease genes are even not always consistently up-/down-regulated, leading to be under-estimated. This problem will seriously influence effective personalized diagnosis or treatment. The expression variance and expression covariance can address such a problem in a network manner. But, these analyses always require multiple samples rather than one sample, which is generally not available in clinical practice for each individual. To extract the common and specific network characteristics for individual patients in this paper, a novel differential network model, e.g. personalized dysfunctional gene network, is proposed to integrate those genes with different features, such as genes with the differential gene expression (DEG), genes with the differential expression variance (DEVG) and gene-pairs with the differential expression covariance (DECG) simultaneously, to construct personalized dysfunctional networks. This model uses a new statistic-like measurement on differential information, i.e., a differential score (DEVC), to reconstruct the differential expression network between groups of normal and diseased samples; and further quantitatively evaluate different feature genes in the patient-specific network for each individual. This DEVC-based differential expression network (DEVC-net) has been applied to the study of complex diseases for prostate cancer and diabetes. (1) Characterizing the global expression change between normal and diseased samples, the differential gene networks of those diseases were found to have a new bi-coloured topological structure, where their non hub-centred sub-networks are mainly composed of genes/proteins controlling various biological processes. (2) The differential expression variance/covariance rather than differential expression is new informative sources, and can be used to identify genes or gene-pairs with discriminative power, which are ignored by traditional methods. (3) More importantly, DEVC-net is effective to measure the expression state or activity of different feature genes and their network or modules in one sample for an individual. All of these results support that DEVC-net indeed has a clear advantage to effectively extract discriminatively interpretable features of gene/protein network of one sample (i.e. personalized dysfunctional network) even when disease samples are heterogeneous, and thus can provide new features like gene-pairs, in addition to the conventional individual genes, to the analysis of the personalized diagnosis and prognosis, and a better understanding on the underlying biological mechanisms. Electronic supplementary material The online version of this article (doi:10.1186/s12967-015-0546-5) contains supplementary material, which is available to authorized users.

Lung disease is the major cause of death and hospitalization worldwide. Transcription factors such as transcription factor 7 (TCF7) are involved in the pathogenesis of lung diseases. TCF7 is important for T cell development and differentiation, embryonic development, or tumorogenesis. Multiple TCF7 isoforms can be characterized by the full-length isoform (FL-TCF7) as a transcription activator, or dominant negative isoform (dn-TCF7) as a transcription repressor. TCF7 interacts with multiple proteins or target genes and participates in several signal pathways critical for lung diseases. TCF7 is involved in pulmonary infection, allergy or asthma through promoting T cells differentiating to Th2 or memory T cells. TCF7 also works in tissue repair and remodeling after acute lung injury. The dual roles of TCF7 in lung cancers were discussed and it is associated with the cellular proliferation, invasion or metastasis. Thus, TCF7 plays critical roles in lung diseases and should be considered as a new therapeutic target.

Background Regulatory T cells (Tregs) and B cells (Bregs) play an important role in the development of lung cancer. The present study aimed to investigate the phenotype of circulating Tregs and Bregs in patients with lung cancer and explore potential mechanism by which lung cancer cells act on the development of both. Methods Patients with lung cancer (n = 268) and healthy donors (n = 65) were enrolled in the study. Frequencies of Tregs and Bregs were measured by flow cytometry with antibodies against CD4, CD25, CD127, CD45RA, CD19, CD24, CD27 and IL-10 before and after co-cultures. qRT-PCR was performed to evaluate the mRNA levels of RANTES, MIP-1α, TGF-β, IFN-γ and IL-4. Results We found a lower frequency of Tregs and a higher frequency of Bregs in patients with lung cancer compared to healthy donors. Co-culture of lung cancer cells with peripheral blood mononuclear cells could polarize the lymphocyte phenotype in the similar pattern. Lipopolysaccharide (LPS)-stimulated lung cancer cells significantly modulated regulatory cell number and function in an in vitro model. Conclusion We provide initial evidence that frequencies of peripheral Tregs decreased or Bregs increased in patients with lung cancer, which may be modulated directly by lung cancer cells. It seems cancer cells per se plays a crucial role in the development of tumor immunity. Electronic supplementary material The online version of this article (doi:10.1186/s12967-014-0304-0) contains supplementary material, which is available to authorized users.

Single cell transcriptome defined as the entire RNA or polyadenylated products of RNA polymerase II on a cell can describe the gene regulation networks responsible for physiological functions, behaviours, and phenotypes in response to signals and microenvironmental changes. Single cell transcriptome/sequencing has the special power to investigate small groups of differentiating cells, circulating tumour cells, or tissue stem cells. A large number of factors may influence the extent of single-cell heterogeneity within a system. It is the opportunity that the single-cell sequencing can be used for the identification of genetic changes in rare cells, e.g. cancer and tissue stem cells, in clinical samples. The methodologies of single-cell sequencing have been improved and developed with the increase of the understanding and attention. The clinical research and application of the single cell sequencing analysis are expected to identify and validate disease-specific biomarkers, network biomarkers, dynamic network biomarkers. The single cell research and value will be also dependent upon the understanding of genomic heterogeneity, planning and design of study protocol, representative of selected and targeted cells, and sensitivity and repeatability of the methodology. The single cell sequencing can be used to develop new diagnostics, monitor disease progresses, measure responses to therapies, and predict the prognosis of patients, although there are still a large number of challenges and difficulties to be faced. It would be more values and specificities of the single cell sequencing to integrate with the function of cells, organs, and systems of the body, the clinical phenotypes of patients, and the description of clinical bioinformatics.

Translational science consists of research and development that integrates multiple resources to expedite the successful treatment of disease. The International Park of Translational BioMedicine (IPTBM) is currently being developed within the interface between Zhejiang Province and Shanghai Municipality. IPTBM has been designed to pioneer comprehensive biomedical research that spans the continuum from the education of young scientists to providing the infrastructure necessary for clinical testing and direct observation to better understand human biology while promoting viable commercial results within a vibrant biotechnology community. IPTBM’s goal is to attract global partners organized around five fundamental pillars: 1) Institutional Development, 2) Project Implementation, 3) Development and Production, 4) Investment and 5) Regulatory Clusters to address the needs of an international platform of scientists, institutes, universities, commercial enterprises, investors, politicians, and other stakeholders. The IPTBM differs from existing models including CTSA’s (US, NIH) technology because of its comprehensive approach to merge education, research, innovation, and development to translate clinical and public health needs into target-oriented and cost-efficient projects.

Disease biomarkers are defined to diagnose various phases of diseases, monitor severities of diseases and responses to therapies, or predict prognosis of patients. Disease-specific biomarkers should benefit drug discovery and development, integrate multidisciplinary sciences, be validated by molecular imaging. The opportunities and challenges in biomarker development are emphasized and considered. The Journal of Translational Medicine opens a new Section of Disease Biomarkers to bridge identification and validation of gene or protein-based biomarkers, network biomarkers, dynamic network biomarkers in human diseases, patient phenotypes, and clinical applications. Disease biomarkers are also important for determining drug effects, target specificities and binding, dynamic metabolism and pharmacological kinetics, or toxicity profiles.

Background Inducing donor-specific tolerance in renal transplant patients could potentially prevent allograft rejection and calcineurin inhibitor nephrotoxicity. Combined kidney and hematopoietic stem cell transplant from an HLA-matched donor is an exploratory and promising therapy to induce immune tolerance. Investigtion of molecular mechanisms involved in the disease is needed to understand the potential process of cell therapy and develop strategies to prevent this immunologic rejection. Methods We enrolled nine patients in a clinical study in which cryopreserved donor hematopoietic stem cells were infused on days 2, 4, and 6 after kidney transplantation. One month post-transplant, 4 plasma samples were collected from combined transplants (C + Tx), and 8 plasma samples from patients with kidney transplantation alone (Tx). High abundance proteins in plasma were depleted and the two-dimensional liquid chromatography-tandem mass spectrometry coupled with iTRAQ labeling was utilized to identify the protein profiling between the two groups. Clusters of up- and down-regulated protein profiles were submitted to MetaCore for the construction of transcriptional factors and regulation networks. Results and Discussion Among the 179 identified proteins, 65 proteins were found in C + Tx with at least a 2-fold change as compared with Tx. A subset of proteins related to the complement and coagulation cascade, including complement C3a,complement C5a, precrusors to fibrinogen alpha and beta chains,was significantly downregulated in C + Tx. Meanwhile, Apolipoprotein-A1(ApoA1), ApoC1, ApoA2, ApoE, and ApoB were significantly lower in Tx compared to C + Tx. Gene ontology analysis showed that the dominant processes of differentially expressed proteins were associated with the inflammatory response and positive regulation of plasma lipoprotein particle remodeling. Conclusions Thus, our study provides new insight into the molecular events in the hematopoietic stem cell-induced immunologic tolerance.

The testicular yolk sac tumor (TYST) is the most common neoplasm originated from germ cells differentiated abnormally, a major part of pediatric malignant testicular tumors. The present study aimed at developing and validating the in vitro and vivo models of TYST and evaluating the sensitivity of TYST to treatments, by cloning human TYST cells and investigating the histology, ultra-structure, growth kinetics and expression of specific proteins of cloned cells. We found biological characteristics of cloned TYST cells were similar to the yolk sac tumor and differentiated from the columnar to glandular-like or goblet cells-like cells. Chromosomes for tumor identification in each passage met nature of the primary tumor. TYST cells were more sensitive to all-trans-retinoic acid which had significantly inhibitory effects on cell proliferation. Cisplatin induced apoptosis of TYST cells through the activation of p53 expression and down-regulation of Bcl- expression. Thus, we believe that cloned TYST cells and the animal model developed here are useful to understand the molecular mechanism of TYST cells and develop potential therapies for human TYST.

Background Intratumoral and circulating regulatory T cells (Tregs) have been shown to be critical in the pathogenesis of hepatocellular carcinoma (HCC). However there is limited knowledge on the alterations of regulatory B cells (Bregs). We here investigated perioperative dynamic alterations of peripheral circulating Tregs and Bregs in HCC patients to reveal the relationship between regulatory lymphocytes and its clinical implications. Methods 36 patients with HCC, 6 with chronic hepatitis B infection and 10 healthy donors were enrolled for this study. Frequencies of peripheral Tregs and Bregs were measured by flow cytometry with antibodies against CD4, CD25, CD127, CD19 and IL-10 before, and after radical surgery. Then, clinical informatics of HCC patients was achieved through Digital Evaluation Score System (DESS) for the assessment of disease severity. Finally, we analysed correlations between digitalized clinical features and kinetics of circulating regulatory lymphocytes. Results Level of circulating CD4+CD25+CD127- Tregs in HCC patients was significantly lower than that in healthy donors and patients with chronic hepatitis B infection before surgery, but was increased after surgery. Preoperative level of CD19+ IL-10+ Bregs in HCC patients was also significantly lower than the other groups. However it dramatically was elevated right after surgery and remained elevated compared to controls (about 7 days after surgery, P = 0.04). Frequency of circulating Tregs was correlated with circulating leukocytes, ferritin, and clinical features suggesting tumor aggressiveness including portal vein thrombosis, hepatic vein involvement and advanced clinical stages. Frequency of circulating Bregs was associated with Hepatitis B e Antigen (HBeAg) and Hepatitis B virus (HBV) DNA copy number. In addition, DESS was significantly and positively correlated with other staging systems. Conclusion Frequencies of peripheral Tregs and Bregs in HCC patients increased after surgery. These results suggest that a postoperative combination of therapies against Tregs and Bregs may be beneficial for better outcome of HCC patients after resection.

Background Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) is an early characteristic of multiple organ dysfunction, responsible for high mortality and poor prognosis in patients. The present study aims to evaluate therapeutic effects and mechanisms of pyrrolidine dithiocarbamate (PDTC) on ALI. Methods Alveolar-arterial oxygen difference, lung tissue edema and compromise, NF-κB activation in polymorphonuclear neutrophil (PMN), and systemic levels of tumor necrosis factor-alpha (TNFa) and intercellular adhesion molecule-1 (ICAM-1) in rabbits induced by the intravenous administration of lipopolysaccharide (LPS) and treated with PDTC. Production of TNFa and IL-8, activation of Cathepsin G, and PMNs adhesion were also measured. Results The intravenous administration of PDTC had partial therapeutic effects on endotoxemia-induced lung tissue edema and damage, neutrophil influx to the lung, alveolar-capillary barrier dysfunction, and high systemic levels of TNFa and ICAM-1 as well as over-activation of NF-κB. PDTC could directly and partially inhibit LPS-induced TNFa hyper-production and over-activities of Cathepsin G. Such inhibitory effects of PDTC were related to the various stimuli and enhanced through combination with PI3K inhibitor. Conclusion NF-κB signal pathway could be one of targeting molecules and the combination with other signal pathway inhibitors may be an alternative of therapeutic strategies for ALI/ARDS.

Translational Medicine is an emerging area comprising multidisciplinary Research from basic sciences to medical applications well summarized by the Bench-to-Beside concept; this entails close collaboration between clinicians and basic scientists across institutes. We further clarified that Translational Medicine should be regarded as a two-way road: Bench-to-Bedside and Bedside-to-Bench, to complement testing of novel therapeutic strategies in humans with feedback understanding of how they respond to them. It is, therefore, critical and important to define and promote Translational Medicine among clinicians, basic Researchers, biotechnologists, politicians, ethicists, sociologists, investors and coordinate these efforts among different Countries, fostering aspects germane only to this type of Research such as, as recently discussed, biotechnology entrepreneurship. Translational Medicine as an inter-disciplinary science is developing rapidly and widely and, in this article, we will place a special emphasis on China.

Inflammatory factors play a vital role in the progression of liver cancer, although exact factors and related mechanisms still remain unclear. The present study aimed at screening inflammatory factors related to liver cancer metastasis and investigating the potential mechanism by which cancer cells are recruited. We screened and validated inflammatory factors by microarray and RT-PCR. Small interfering RNA (siRNA) and recombinant protein were used to assess CXCL5 effects on the movement of liver cancer cells (LCCs). Our screening microarray demonstrated over-expression of CXCL5 in LCCs with high metastatic potentials. CXCL5 increased LCCs migration and invasion, probably through autocrine and paracrine mechanisms. CXCL5-CXCR2 and ERK1/2 pathways could play critical roles in the regulation of LCCs migration. Our data indicates that LCCs per se may act as the producer and receptor of CXCL5 responsible for liver cancer migration and invasion.

Translational medicine entails not only “from-bench-to-bedside” but also preventive medicine. The present article proposes a conceptual framework of translational research from scientific research to health care policy and public health policy. We highlight the importance of translational medicine to bridge between research and policy and share our experience of translating medical research to public health policy in China as well as obstacles and challenges we are facing in the translation process.

Background The target-controlled infusion-III (SLOG/TCI-III) system was derived from a model set up by the local pediatric population for target control infusion of propofol. Methods The current study aimed at evaluating the difference between target concentrations of propofol and performance, which was measured using the SLOG/TCI-III system in children. Thirty children fulfilling the I-II criteria according to American Society of Anesthesiology were enrolled in the study. The target plasma concentration of propofol was fed into the SLOG/TCI-III system and compared with the measured concentrations of propofol. Blood samples were collected and analyzed by high performance liquid chromatography with fluorescence detector. The performance error (PE) was determined for each measured blood propofol concentration. The performances of the TCI-III system were determined by the median performance error (MDPE), the median absolute performance error (MDAPE), and Wobble (the median absolute deviation of each PE from the MDPE), respectively. Results Concentration against target concentration showed good linear correlation: concentration = 1.3428 target concentration - 0.2633 (r = 0.8667). The MDPE and MDAPE of the pediatric system were 10 and 22%, respectively, and the median value for Wobble was 24%. MDPE and MDAPE were less than 15 and 30%, respectively. Conclusions The performance of TCI-III system seems to be in the accepted limits for clinical practice in children.

Background Cough is one of the most common respiratory symptoms and is well characterized in specialized cough clinics with high success rates of diagnosis and treatment. However, there is a paucity of data regarding cough in primary care settings. The present study aimed at investigating clinical epidemiology of cough through a national study of two questionnaire surveys sent to primary care physicians in China. Methods Approximately 18,000 subjects recruited were having daytime or night symptoms of cough and diagnoses of respiratory disease from February 2005 to April 2006 as Survey 1 and from June 2007 to December 2007 as Survey 2. Patients suffering from respiratory malignancy, hyperthyroidism, hypertension, heart disease, diabetes, severe hypohepatia or renal dysfunction, pregnancy, possible pregnancy or lactation, neutropenia were not eligible. Information regarding demography, history of allergies, symptomatic profile, treatment and curative effects for cough was elicited. Results 8216 questionnaires were collected in Survey 1 and 9711 in Survey 2. The mean values of ages were 25.7 and 22.3 years old, respectively. Symptoms included expectoration (74% and 76%), wheeze (59% and 74%), breathlessness (22% and 26%), chest pain (9% and 13%) and fever (15% and 18%). About 15% and 23% patients had hypersusceptibility, of whom 6% to 17% had a family history. More than 50% of the cases had histories of allergic rhinitis, asthma, conjunctivitis or atopic dermatitis. Asthma, COPD, and bronchitis were dominant etiologies of cough. Procaterol or the combination of antibiotics and steroids were used as the treatment. Conclusion Causes and outcomes of cough differed with ages and time in this particular national study, while successful and precise diagnosis and management of cough in primary care settings need to be further improved in China.

Background Asthma is prone to Th2-mediated chronic airway inflammation. Interleukin-27 (IL-27) is a member of the IL-12 family that promotes the differentiation of Th1 cells and inhibits Th2 cells. We use human/mouse CD4+ T cells to see whether IL-27 could inhibit IL-4 production in vitro and then observe whether IL-27 administration could alleviate allergic airway inflammation in vivo by mice asthma model. Methods We isolated and cultured CD4+ T cells from healthy humans and mice to test whether IL-27 could inhibit IL-4 production under different conditions. In vivo study, the effect of IL-27 was examined using two types of intra-nasal (i.n.) administration: low-dose-multiple-times prevention or high-dose-limited-times treatment in murine asthma models. The expression levels of signal transducer and activator of transcription-1 (STAT1) and growth arrest and DNA damage 45-γ (GADD45γ)/p38 mitogen activated protein kinase (p38 MAPK) in lung tissues were measured using qPCR and Western blotting. Results In vitro, although IL-27 could inhibit naïve CD4+ T cell differentiate into Th2 cells, but it could not redifferentiate already committed Th2 cells. In vivo, preventative administration of IL-27 attenuated allergic inflammation and airway hyperreactivity, whereas treatment group had no significant effect. In the asthma group, the phosphorylation of STAT1 was impaired, while GADD45γ and p38 MAPK exhibited no obvious changes. Preventative administration of IL-27 could either reverse the impairment of STAT1 or strengthen the expression of GADD45γ and p38 MAPK, whereas treatment group had no significant effect. Conclusions Preventative administration of IL-27 improved the pathological changes in mouse asthma models via both the STAT1 and GADD45γ/p38 MAPK pathways while therapeutic administration of IL-27 had no significant effect, which may be due to the presence of already differentiated Th2 cells in asthmatic airways that resist IL-27 inhibition. Electronic supplementary material The online version of this article (doi:10.1186/s12967-016-1039-x) contains supplementary material, which is available to authorized users.

Background Telocytes, a new type of interstitial cells, have been identified in many organs in mammals. The present studies aimed at investigating the ultrastructure, distribution and interactions of telocytes with surrounding cells in the urinary system of rats, to confirm the existence of telocytes in kidneys, ureter and urinary bladder. Methods Samples of kidney, ureter, or urinary bladder were harvested for the ultrastructure by the electron microscope. The primary culture of telocytes was performed to investigate the dynamic alterations. Results Telocytes mainly located in the sub-capsular space of kidney, or between smooth muscle bundles and in the lamina propria of ureter and urinary bladder. Telocytes established numerous contacts with macrophages in the sub-capsular space of kidney, or with smooth muscle cells, nerve endings as well as blood capillaries in the ureter and urinary bladder. The complete morphology of telocytes with telopodes was observed clearly through the primary cell culture from the kidney tissues of rats. Conclusions Our data evidenced the existence of telocytes in the urinary system, which may contribute to the tissue reparation and regeneration.

Disease biomarkers are defined to diagnose various phases of diseases, monitor severities of diseases and responses to therapies, or predict prognosis of patients. Disease-specific biomarkers should benefit drug discovery and development, integrate multidisciplinary sciences, be validated by molecular imaging. The opportunities and challenges in biomarker development are emphasized and considered. The Journal of Translational Medicine opens a new Section of Disease Biomarkers to bridge identification and validation of gene or protein-based biomarkers, network biomarkers, dynamic network biomarkers in human diseases, patient phenotypes, and clinical applications. Disease biomarkers are also important for determining drug effects, target specificities and binding, dynamic metabolism and pharmacological kinetics, or toxicity profiles.

Background Betacellulin (BTC), a member of the epidermal growth factor (EGF) family, binds and activates ErbB1 and ErbB4 homodimers. BTC was expressed in tumors and involved in tumor growth progression. CXCL8 (interleukin-8) was involved in tumor cell proliferation via the transactivation of the epidermal growth factor receptor (EGFR). Materials and methods The present study was designed to investigate the possible interrelation between BTC and CXCL8 in human lung cancer cells (A549) and demonstrated the mechanisms of intracellular signals in the regulation of both functions. Bio-behaviors of A549 were assessed using Cell-IQ Alive Image Monitoring System. Results We found that BTC significantly increased the production of CXCL8 through the activation of the EGFR-PI3K/Akt-Erk signal pathway. BTC induced the resistance of human lung cancer cells to TNF-α/CHX-induced apoptosis. Treatments with PI3K inhibitors, Erk1/2 inhibitor, or Erlotinib significantly inhibited BTC-induced CXCL8 production and cell proliferation and movement. Conclusion Our data indicated that CXCL8 production from lung cancer cells could be initiated by an autocrine mechanism or external sources of BTC through the EGFR–PI3K–Akt–Erk pathway to the formation of inflammatory microenvironment. BTC may act as a potential target to monitor and improve the development of lung cancer inflammation.