CC chemokine ligand-2 (CCL2), a proinflammatory chemokine that mediates chemotaxis of multiple immune cells, plays a crucial role in the tumor microenvironment (TME) and promotes tumorigenesis and development. Recently, accumulating evidence has indicated that CCL2 contributes to the development of drug resistance to a broad spectrum of anticancer agents, including chemotherapy, hormone therapy, targeted therapy, and immunotherapy. It has been reported that CCL2 can reduce tumor sensitivity to drugs by inhibiting drug-induced apoptosis, antiangiogenesis, and antitumor immunity. In this review, we mainly focus on elucidating the relationship between CCL2 and resistance as well as the underlying mechanisms. A comprehensive understanding of the role and mechanism of CCL2 in anticancer drug resistance may provide new therapeutic targets for reversing cancer resistance.
The long non-coding RNA (lncRNA) H19 acts as a competitive endogenous RNA (ceRNA) of miR-29b-3p and has been reported to exert pro-tumorigenic roles in several cancer types.However, the role of lncRNA H19 in lung cancer is not fully understood. Here, we investigated the role of the lncRNA H19/microRNA-29b-3p (miR-29b-3p)/high mobility group box 1 (HMGB1) signaling pathway in lung cancer cell growth using 293T, NCI-H1975, Calu-3 and 2BS cell lines. Cell viability was determined using a cell counting kit-8 (CCK-8) assay, while apoptosis and cell cycle distribution were assessed by flow cytometry. Cell migration was detected using a wound healing assay. Cell invasion was evaluated by transwell assay. The expression of lncRNA H19, miR-29b-3p, HMGB1, toll-like receptor 4 (TLR4), and matrix metallopeptidase 9 (MMP-9) was measured by fluorescence quantitative PCR or western blotting. We demonstrated that miR-29b-3p could directly bind to both lncRNA H19 and HMGB1 by dual-luciferase reporter assay. Three shRNAs targeting lncRNA H19 (shlncRNA H19) were designed, and shlncRNA H19-2 was selected to investigate the function of lncRNA H19 in tumor cell biology. Compared with controls, lung cancer cells expressing shlncRNA H19 exhibited decreased proliferation, cell-cycle arrest at the G1 phase, increased levels of cell apoptosis, and reduced migration and invasion. Moreover, shlncRNA H19 upregulated the expression of miR-29b-3p and reduced the protein expression of HMGB1, TLR4, and MMP-9 in lung cancer cells. Together, our data indicate that the lncRNA H19/miRNA-29b-3p/HMGB1 signaling axis is involved in the regulation of lung cancer cell growth.
Gastric cancer (GC) is the third leading cause of cancer-related deaths worldwide. However, there are still no reliable biomarkers for the prognosis of this disease. This study aims to construct a robust protein-based prognostic prediction model for GC patients. The protein expression data and clinical information of GC patients were downloaded from the TCPA and TCGA databases, and the expressions of 218 proteins in 352 GC patients were analyzed using bioinformatics methods. Additionally, Kaplan–Meier (KM) survival analysis and univariate and multivariate Cox regression analysis were applied to screen the prognosis-related proteins for establishing the prognostic prediction risk model. Finally, five proteins, including NDRG1_pT346, SYK, P90RSK, TIGAR, and XBP1, were related to the risk prognosis of gastric cancer and were selected for model construction. Furthermore, a significant trend toward worse survival was found in the high-risk group (p = 1.495 × 10−7). The time-dependent ROC analysis indicated that the model had better specificity and sensitivity compared to the clinical features at 1, 2, and 3 years (AUC = 0.685, 0.673, and 0.665, respectively). Notably, the independent prognostic analysis results revealed that the model was an independent prognostic factor for GC patients. In conclusion, the robust protein-based model based on five proteins was established, and its potential benefits in the prognostic prediction of GC patients were demonstrated.
ObjectiveThis study investigated whether differences in the induction chemotherapy (IC) cycle number and adjuvant chemotherapy (AC) affect survival outcomes in patients with locally advanced nasopharyngeal carcinoma (LA-NPC).MethodsThe survival outcomes of 386 consecutive LA-NPC patients treated between January 2015 and March 2018 were retrospectively analyzed. Univariate and multivariate analyses were used to compare treatment groups defined by IC< 3 or ≥3 IC cycles followed by radiotherapy with or without AC (i.e., IC<3+AC, IC<3+non-AC, IC≥3+AC, and IC≥3+non-AC groups).ResultsThe median follow-up time was 53 months (range: 2-74 months) and the median number of IC cycles was 2 (range: 1-6 cycles). The 3-year overall survival (OS) rate was significantly higher in patients with IC≥3 cycles compared to IC<3 cycles (95.7% vs. 90.3%, P=0.020). Multivariate analysis indicated that the IC cycle number is an independent factor for OS (hazard ratio=0.326, P=0.007). Furthermore, patients in the IC<3+AC group had a better OS rate than those in the IC<3+non-AC group (91.6% vs. 79.1%, P=0.030), indicating that AC positively affected OS in patients with IC<3. However, no significant difference in the OS rate was found between IC≥3+non-AC and IC≥3+AC groups (92.1% vs. 94.6%, P =0.550).ConclusionThe IC cycle number appears to be an independent prognostic factor for higher OS in LA-NPC patients who received ≥3 cycles. Sequential AC after IC plus radiotherapy may improve OS in patients with IC<3 cycles.
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