ObjectiveFibroblast activation protein (FAP) plays a vital role in tumor invasion and metastasis. Previous studies have reported its prognostic value in different tumors. However, the results of these reports remain controversial. In this study, a meta-analysis was performed to clarify this issue.MethodsA search of the PubMed, Embase and CNKI databases was conducted to analyze relevant articles. The outcomes included the relations between FAP expression and histological differentiation, tumor invasion, lymph node metastasis, distant metastasis and overall survival (OS). Sensitivity analysis by FAP expression in different cells and tumor types were further subjected to sensitivity analyses as subgroups. Pooled odds ratios (ORs) and hazard ratios (HRs) were evaluated using the random-effects model.ResultsThe global analysis included 15 studies concerning various solid tumors. For global analysis, FAP overexpression in tumor tissue displayed significant associations with poor OS and tumor progression (OS: HR = 2.18, P = 0.004; tumor invasion: OR = 4.48, P = 0.007; and lymph node metastasis: OR = 3.80, P = 0.004). The subgroup analyses yielded two notable results. First, the relation between FAP overexpression and poor OS and tumor lymph node metastasis was closer in the patients with FAP expression in tumor cells. Second, the pooled analyses of colorectal cancers or pancreatic cancers all indicated that FAP overexpression was associated with a detrimental OS (HR: 1.72, P = 0.009; HR: 3.18, P = 0.005, respectively). The magnitude of this effect was not statistically significant compared with that in patients with non-colorectal cancers or non-pancreatic cancers. These analyses did not display a statistically significant correlation between FAP expression and histological differentiation and distant metastasis in all of the groups.ConclusionsFAP expression is associated with worse prognosis in solid tumors, and this association is particularly pronounced if FAP overexpression is found in the tumor cells rather than the stroma.
We intended to study the mechanism of the inhibitory action of curcumin on human non-small cell lung cancer A549 cell. The cell growth was determined by CCK-8 assay, and the results indicated that curcumin inhibited the cell proliferation in a concentration dependent manner. And to further confirm the relative anti-cancer mechanism of curcumin, RT-PCR was carried out to analysis the expression of relative apoptotic proteins Bax, Bcl-2. We found that curcumin could up-regulate the expression of Bax but down-regulate the expression of Bcl-2 in A549 cells. In addition, curcumin affect the mitochondrial apoptosis pathway. These results suggested that curcumin inhibited cancer cell growth through the regulation of Bcl-2/Bax and affect the mitochondrial apoptosis pathway.
Lung cancer continues to be an enormous burden on current health care systems throughout the world, with more than a million deaths every year. Previous studies have shown that interleukin-22 (IL-22) promotes survival and resistance to chemotherapy in human lung cancer cells. However, the association of IL-22 expression with recurrence of lung cancer is still unclear. In this study, we found that expression of IL-22 was upregulated in tumor tissues and serum from patients with recurrent non-small cell lung cancer (NSCLC) as compared to primary NSCLC samples. Treatment with IL-22 promoted cell proliferation and enhanced migration and invasion in A549 and H125 cell lines. Furthermore, we revealed that phosphorylation of STAT3 and AKT was highly induced by treatment with IL-22 via IL-22R1. IL-22R1 was also consistently overexpressed in recurrent NSCLC tissues. Finally, we found that siRNA-mediated depletion of IL-22R1 completely abrogated the effects of IL-22 treatment on cell proliferation and migration activity in NSCLC cell lines. Our findings indicate that IL-22 and IL-22R1 may be novel therapeutic targets for treatment of advanced NSCLC.
Family with sequence similarity 83, member A (FAM83A), as a potential tumor promoter, was reported to contribute to the progression of several malignant tumors. However, the significance of FAM83A in invasion and metastasis of non-small cell lung cancer (NSCLC) remains largely unknown. In this study, we found that FAM83A expression was significantly increased in NSCLC tissues. High expression of FAM83A was positively associated with tumor metastasis and poor survival of NSCLC patients. Functional experiments revealed that FAM83A knockdown could suppress NSCLC cell migration and invasion both in vivo and in vitro. While opposite results were observed in FAM83A-transfected cells. Mechanically, we found that FAM83A promoted NSCLC cell migration and invasion by inducing epithelial-mesenchymal transition (EMT) via PI3K/ATK/Snail signaling. Rescue experiment demonstrated that inhibition of either AKT or Snail could partially counteract the promoting effect of FAM83A overexpression in NSCLC metastasis. Taken together, our findings are the first time to demonstrate that increased expression of FAM83A in NSCLC was correlated with EMT and tumor metastasis, which may provide a novel therapeutic target in NSCLC treatment.
Sal-like 4(SALL4) is significant for maintaining self-renewal and pluripotency in embryonic stem cells, cancer cells and perhaps even cancer stem cells. The expression of SALL4 has been recorded in various kinds of cancers and is deemed to have a clinical value for diagnosis. However, little information on SALL4 expression has been illustrated in breast cancer. In this study, the expression of SALL4 was scrutinized by immunohistochemical analysis in breast invasive ductal carcinoma in a large cohort of 160 patients. High cytoplasmic expression of SALL4 was detected in breast cancer tissues compared with normal adjacent tissues. High SALL4 expression was associated with advanced tumor invasion (p = 0.019), lymph node stage (p = 0.027), ER (p = 0.030), PR (p = 0.037), HER2 (p = 0.019) and TNBC (p = 0.007) in overall patients. Interestingly, in Kaplan-Meier analysis, breast cancer patients with high expression of SALL4 demonstrated a worse OS. Both univariate and multivariate analysis illustrated that examination of SALL4 was of great prognostic value in OS. Thus, our data showed that high cytoplasmic expression of SALL4 was considered to be an independent prognostic indicator for breast invasive ductal carcinoma.
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