Long intergenic non-coding RNAs (lincRNAs) are long non‑coding transcripts from the intergenic regions of annotated protein‑coding genes. lincRNA cyclooxygenase 2 (Cox2) is an early‑primary response gene regulated by the NF‑κB signaling pathway in macrophages. It was found that lincRNACox2 was significantly increased in patients with the Mycobacterium tuberculosis (M. tuberculosis) H37Ra strain infection and macrophages, using reverse transcription-quantitative PCR (RT‑qPCR). ELISA, western blotting and RT‑qPCR results indicated that the inflammatory response factors tumor necrosis factor‑α, interferon‑γ, interleukin‑6, Cox2 and inducible nitric oxide synthase were significantly increased in H37Ra infected macrophages. In addition, the inflammatory regulating proteins NF‑κB and Stat3 were significantly increased in H37Ra infected macrophages but decreased in lincRNACox2 knockdown macrophages infected with H37Ra. Moreover, the knockdown of lincRNACox2 increased the apoptotic rate of H37Ra infected macrophages and facilitated the proliferation of H37Ra. Collectively, the present results suggested that lincRNACox2 may be required for the activation of NF‑κB and Stat3, in order to regulate inflammatory responses involved in resistance to M. tuberculosis infection.The existence of cancer stem cells (CSCs) is considered to be the main reason for chemoresistance, metastasis and the ultimate failure of treatment in hepatocellular carcinoma (HCC). However, there are a few chemical agents that may inhibit CSCs. The present study identified that 4,4'‑bond secalonic acid D (4,4'‑SAD), a compound isolated from the marine‑derived fungus Penicillium oxalicum, inhibited the growth of side population (SP) cells isolated from human liver cancer cell lines PLC/PRF/5 and HuH‑7 by attenuating the expression of ATP‑binding cassette superfamily G member 2. Furthermore, the results of wound healing, Transwell, western blotting and reverse transcription‑quantitative PCR assays demonstrated that 4,4'‑SAD suppressed the invasion and migration of SP cells by downregulating matrix metallopeptidase 9 (MMP‑9) and upregulating the antagonist tissue inhibitor of metalloproteinases 1 in vitro. Moreover, in vivo study results found that 4,4'‑SAD had anti‑lung metastasis efficacy via the decrease of MMP‑9 expression in the H22 HCC model of Kunming mice. Therefore, the present study identified the potential of 4,4'‑SAD as a promising candidate for the treatment of advanced liver cancer.Runt‑related transcription factor 3 (RUNX3) is a candidate tumor suppressor, and its inactivation may play a crucial role in the carcinogenesis process of numerous cancer types, including esophageal squamous cell carcinoma (ESCC). We previously revealed that RUNX3 inactivation was correlated with lymph node metastasis (LNM) and ESCC recurrence. However, the exact mechanisms of this process are still under investigation. The aim of the present study was to examine the potential roles and underlying molecular mechanisms of RUNX3 in ESCC metastasis and the epithelial‑mesenchymal transition (EMT). According to the results, RUNX3 expression in ESCC tissue was significantly reduced compared with that in adjacent normal tissue (0.50±0.20 vs. 0.83±0.16; P less then 0.001). In addition, statistical analysis revealed a close association between decreased RUNX3 expression and T status (P=0.027) and LNM (P=0.017) in ESCC patients. Pearson's correlation coefficient analysis was then used to evaluate correlations between RUNX3 and EMT‑related marker expression. The results revealed that RUNX3 expression in ESCC tissues was negatively correlated with the expression of N‑cadherin (r=‑0.429; P less then 0.01) and Snail (r=‑0.364; P less then 0.01) and positively correlated with the expression of E‑cadherin (r=0.580; P less then 0.01). Moreover, Eca109 and EC9706 cell invasion, migration, MMP‑9 expression and EMT were significantly inhibited by RUNX3 overexpression. Notably, further analysis revealed that RUNX3 overexpression markedly inhibited the phosphorylation of Smad2/3; RUNX3‑overexpressing cells also displayed less sensitivity to TGF‑β1‑induced EMT than control cells. https://www.selleckchem.com/products/ono-7475.html Thus, RUNX3 may inhibit the invasion and migration of ESCC cells by reversing EMT through TGF‑β/Smad signaling and may be useful as a therapeutic target.The epidermal growth factor receptor‑tyrosine kinase inhibitor (EGFR‑TKI), gefitinib, is used widely to treat non‑small cell lung cancer (NSCLC) with EGFR‑activating mutations. Unfortunately, the acquired drug resistance promoted by epithelial‑mesenchymal transition (EMT) markedly limits the clinical effects and remains a major barrier to a cure. Our previous isobaric tags for relative and absolute quantitation‑based proteomics analysis revealed that the E‑cadherin protein level was markedly upregulated by triptolide (TP). The present study aimed to determine whether TP reverses the gefitinib resistance of human lung cancer cells by regulating EMT. It was revealed that TP combined with gefitinib synergistically inhibited the migration and invasion of lung adenocarcinoma cell line A549; the combination treatment had a significantly better outcome than that of TP and gefitinib alone. Moreover, TP effectively increased the sensitivity of drug resistant A549 cells to gefitinib by upregulating E‑cadherin protein expression and downregulating the MMP9, SNAIL, and vimentin expression levels. The dysregulated E‑cadherin expression of gefitinib‑sensitive cells induced gefitinib resistance, which could be overcome by TP. Finally, TP combined with gefitinib significantly inhibited the growth of xenograft tumors induced using gefitinib‑resistant A549 cells, which was associated with EMT reversal and E‑cadherin signaling activation in vivo. The present results indicated that the combination of TP and TKIs may be a promising therapeutic strategy to treat patients with NSCLCs harboring EGFR mutations.Circulating tumor cells (CTCs), are tumor cells that diffuse into the circulating blood and serve an important role in the progress of cancer. During the early stages of cancer, CTCs undergo an epithelial‑mesenchymal transition and obtain a more invasive phenotype. Subsequently, the tumor cells enter the circulating blood with the aid of immune cells, and enter a dormant state upon reaching distal organs. As the tumor progresses, metastasis may occur under certain conditions. The capture technologies available for CTCs are based on antibody‑based capture, or capture based on the physical properties of CTCs, as well as modern technologies that integrate both these methods. Emerging modern technologies have increased the accuracy and efficiency of tumor cell capture, and have thus improved our understanding of tumor cells, and the molecular mechanisms underlying their properties. CTCs serve an important role in disease progression, prediction of patient prognosis and individualized treatment.