Tumor invasion and metastasis are closely associated with epithelial-mesenchymal transition (EMT). EMT refers to epithelial cells under physiological and pathological conditions that are specific to mesenchymal transition. Curcumin inhibits EMT progression via Wnt signaling. The Wnt signaling pathway is a conservative EMT-related signaling pathway that is involved in the development of various tumors. In the present study, MTS assays were employed to analyze the proliferation of curcumin-treated cells. Naked cuticle homolog 2 (NKD2), chemokine receptor 4 (CXCR4) and antibodies associated with EMT were examined in SW620 colorectal cancer cell lines using western blot analysis and real-time qPCR. NKD2 small-interfering RNA (siRNA) and CXCR4 expression plasmid was synthesized and transfected into the colorectal cancer cell lines, and NKD2 and CXCR4 expression levels were detected. The results showed that curcumin significantly inhibited the proliferation of colorectal cancer cells and upregulated the expression of NKD2 in SW620 colorectal cancer cells and in the xenograft, resulting in the downregulation of key markers in the Wnt signaling. In addition, the progression of ETM was inhibited due to the overexpression of E-cadherin as well as the downregulation of vimentin. Curcumin also inhibited tumor metastasis by downregulating the expression of CXCR4 significantly. The results suggested involvement of the NKD2-Wnt-CXCR4 signaling pathway in colorectal cancer cells. In addition, curcumin is inhibit this signaling and the development of colorectal cancer.

ω-3 polyunsaturated fatty acids (n-3 PUFA), in particular the marine-derived forms eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have been demonstrated to affect cancer cell replication, the cell cycle and cell death. Epidemiological studies have also suggested diets rich in n-3 PUFA were inversely correlated with the development of cancer. In the present study, we explored the effects of DHA and EPA on the proliferation activity and apoptosis of the human lung adenocarcinoma cell line A549. A methyl thiazolyl tetrazolium (MTT) assay was used to detect cell proliferation, apoptosis was detected by flow cytometry and morphological analysis was determined by fluorescence microscopy and transmission electron microscopy. A549 cells were treated with different doses of DHA (40, 45, 50 and 55 µg/ml) or EPA (45, 50, 55 and 60 µg/ml) for 24, 48 and 72 h. The results demonstrated that DHA and EPA significantly suppressed the proliferation of A549 cells and induced apoptosis of A549 cells in a dose- and time-dependent manner. The apoptotic phenomenon was also confirmed by fluorescence microscopy and transmission electron microscopy. Furthermore, compared with the control, the formation of autophagosomes was clearly enhanced in DHA‑ or EPA-treated cells. In conclusion, DHA and EPA inhibited the proliferation of A549 cells and induced cell apoptosis and autophagy, which may provide new safe and effective options for the treatment of lung cancer in the future.

Abstract. Curcumin has been found to exhibit anticancer activity and certain studies have shown that curcumin triggers the apoptosis of human A549 lung adenocarcinoma cells. However, the mechanism underlying curcumin-mediated apoptosis is not completely understood. The present study was designed to investigate the effect of curcumin on the induction of apoptosis and apoptosis-related factors in human A549 lung adenocarcinoma cells. Treatment of A549 cells with curcumin caused a concentration-dependent inhibition of cell growth and an increase in apoptosis, as confirmed by THE MTT assay, flow cytometry and morphology analysis. Curcumin-treatment of A549 cells induced a loss of the mitochondrial membrane potential and increased cytosolic cytochrome c. Furthermore, curcumin-induced apoptosis was accompanied by changes in intracellular oxidative stress-related enzymes, including decreased intracellular reactive oxygen species levels, increased superoxide dismutase and decreased malondialdehyde and 4-hydroxynonenal. In addition, induction of apoptosis was also accompanied by phosphorylation and activation of mitogen-activated protein kinase signaling pathway factors c-Jun N-terminal kinase, p38 and extracellular signal-regulated kinase. IntroductionLung cancer is the main leading cause of cancer-related fatality worldwide, with a rapidly increasing rate in China and other Asian countries (1-4). Chemotherapy is currently the most frequently used treatment for lung cancer and other types of cancer. However, while this method of treatment kills cancer cells, it also destroys some normal cells. Thus, the identification of novel natural compounds with low toxicity and high selectivity for killing cancer cells is a significant area in cancer research (5), and several natural products have been used as alternative treatments for cancer (6,7).Curcumin, a natural and crystalline compound isolated from the plant Curcuma longa, has been widely studied for its anti-inflammatory, antiangiogenic, antioxidant and anticancer effects in Chinese systems of medicine (8,9). Additionally, previous studies have shown that curcumin exhibits antiproliferative and anticarcinogenic properties in a wide variety of cell lines and animals (10,11). Previous studies have demonstrated that curcumin inhibits the growth and apoptosis of human A549 lung adenocarcinoma cells (12)(13)(14). However, the mechanisms of curcumin-induced apoptosis via oxidative stress remain unclear.The physiological status of the reactive oxygen species (ROS) levels can regulate cell proliferation: When intracellular ROS levels are above a certain threshold, ROS inhibit the cell cycle, leading to increased cell apoptosis and necrosis. In the tumor cells it often maintains a higher state of oxidation, with higher levels of oxygen free radicals and lower levels of the antioxidant enzyme activity. This higher oxidation state can activate certain transcription factors and associated genes, such as NF-κB and API, thus, ensuring the survival, proliferation and migration of tumor ...

Abstract. The present study identified that ω-3 long chain polyunsaturated fatty acids (ω-3 PUFAs), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) demonstrate anti-proliferative effects in lung cancer A549 cells. MTS and cytotoxicity assays were conducted to confirm that ω-3 PUFAs induced cell death. Autophagy-associated gene and signaling pathways were also detected. Microtubule-associated protein light chain 3 (LC3) expression was found to be increased subsequent to treatment with DHA and EPA, and the expression of LC3-II was particularly increased. mRFP-GFP-LC3 fluorescence staining and p62 expression levels were used to detect autophagic flux. The present results indicate that DHA and EPA block autophagic flux, suggesting autophagosome accumulation. Subsequent to treatment with DHA and EPA, which interfered with autophagosomes, the expression of Beclin 1 was significantly decreased, while the expression of phosphorylated Akt and phosphorylated mammalian target of rapamycin was significantly increased. Therefore, DHA and EPA exert anti-proliferative effects by inhibiting autophagy in A549 cells, which highlights the potential of DHA and EPA for use in the prevention or treatment of lung cancer. IntroductionLung cancer is the leading cause of cancer-associated mortality worldwide (1), and the five-year survival rate remains extremely poor (2). Overall, ~75-85% of lung cancers cases are non-small cell lung cancer (NSCLC), which includes squamous cell carcinoma, adenocarcinoma and large cell carcinoma. The treatment of lung cancer involves the use of medical therapies such as surgery, radiation, chemotherapy and palliative care (3) in an attempt to successfully treat or reduce the adverse impact of malignant neoplasms originating in lung tissue. Chemotherapeutic agents are the main treatment measures for NSCLC, but the side-effects are usually difficult to tolerate (4).Fish oils are an excellent source of long-chain ω-3 polyunsaturated fatty acids (ω-3 PUFAs), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Fish oil supplements are increasingly recognized by clinical studies to be useful for the treatment of a variety of human afflictions, including cancer (5). Numerous studies reveal evidence for the capability of ω-3 PUFAs to decrease proliferation, exert a pro-apoptotic effect and inhibit angiogenesis in several in vitro models of colon cancer (6-9).A previous study indicated that DHA and EPA inhibit the proliferation of A549 cells and induce apoptosis, with autophagy also being observed under transmission electron microscopy (10). Autophagy is a type of programmed cell death and it is an important process that is involved in various human pathologies. Previous studies suggest that autophagy is important in the regulation of cancer development and progression and also in determining the response of tumor cells to anticancer therapy (11)(12)(13)(14). Several cell signaling pathways are implicated in regulating autophagy, including the phosphatidyl inositol 3-kinase (PI3K)/Akt/...

BackgroundAn increasing number of studies have found that the gut microbiota was related to the occurrence and development of lung cancer. Nonetheless, publication trends and research hotspots in this field remain unknown. The study aimed to perform a bibliometric analysis to systematically identify publication trends and research hotspots in the field of gut microbiota and lung cancer research within a 12-year panorama.MethodsPublications related to the gut microbiota and lung cancer between 1 January 2011 and 25 October 2022 were retrieved from the Web of Science Core Collection (WoSCC) database. The online analytic tool of the WoSCC was used to analyze various bibliometric parameters. The bibliometrics website, CiteSpace, and VOSviewer were used to identify research trends and hotspots.ResultsA total of 375 publications related to the gut microbiota and lung cancer were extracted from WoSCC and identified for analysis. The number of annual publications has grown rapidly since 2018 and reached a peak in 2022. China was the most prolific country in this field, with 120 publications, followed by the United States (114), with the highest H-index of 31. Additionally, France ranked the highest with an average of 133 citations, while the leading institution and journal were the Unicancer and the International Journal of Molecular Sciences, respectively. Interestingly, Routy Bertrand was the most prolific author and also the most cited author in terms of H-index and citations. Reference and keyword burst detection indicated that the research hotspots mainly included 1) the gut microbiota directly affects the efficacy of immunotherapy for lung cancer, 2) the application of different gut bacteria on lung cancer, and 3) the mechanism of the gut microbiota on lung cancer.ConclusionThe findings of this study revealed the general publication trends and evolving research hotspots in the field of gut microbiota and lung cancer at a global level. The research hotspots focused on the clinical application of the gut microbiota combined with immunotherapy in lung cancer and its mechanism. The findings of this study provide new perspectives on the field, which may shed light on a beneficial impact on further etiological studies, diagnosis, and treatment for lung cancer.