Abstract. Leptin is associated with carcinogenesis and progression of various cancers. However, the changes of the serum leptin level in Chinese overweight patients with colon carcinoma and its association with response to treatment in these patients have rarely been investigated. A total of 63 Chinese overweight patients with colon cancer and 40 body mass index-matched control subjects were recruited in the present study. The serum leptin levels of colon cancer patients prior to and 21 days after colectomy, as well as those of healthy controls, were measured and compared. In addition, the focal expression of phosphorylated Akt, mammalian target of rapamycin and 70S6 Kinase (p-Akt, p-mTOR and P-70S6 Kinase) and leptin were determined in the resected specimens and the correlation between serum leptin levels and the focally expressed markers were investigated. The serum leptin levels of colon cancer patients were significantly higher compared with those of the controls (22.67±12.56 vs. 12.68±7.8 ng/ml, respectively; P<0.05). Moreover, the leptin levels decreased after the operation when compared to the preoperative levels (18.67±8.54 vs. 22.67±12.56 ng/ml, respectively; P<0.05). In addition, there was a significant correlation between the serum leptin levels and the focal expression of p-Akt, p-mTOR, P-70S6 Kinase and leptin (P<0.05). In conclusion, the leptin levels were elevated in Chinese overweight patients with colon cance these levels decreased following colectomy, indicating that leptin may be associated with colon carcinogenesis. Thus, serum leptin level may be used for early diagnosis and for monitoring the response to treatment of colon carcinoma in overweight Chinese patients.
Background Accumulating evidence suggests that circular RNAs (circRNAs) play important regulatory roles in non‐small cell lung cancer (NSCLC). At present, we aimed to explore the regulatory role of has_circ_0003528 (circ_0003528) in NSCLC. Methods Alterations of circ_0003528 expression in NSCLC samples and cell lines were detected by real‐time quantitative polymerase chain reaction (RT‐qPCR). Impacts of circ_0003528 on NSCLC cell malignant transformation were analyzed by 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐Diphenyltetrazolium Bromide (MTT), 5‐ethynyl‐2′‐deoxyuridine (EdU), flow cytometry, transwell invasion, and tube formation assays. Epithelial‐mesenchymal transition (EMT)‐related markers were detected with western blotting. Pro‐inflammatory cytokines were detected by Enzyme‐linked immunosorbent assay (ELISA). The regulation mechanism of circ_0003528 was verified by dual‐luciferase reporter and RNA pull‐down assays. The tumorigenesis role of circ_0003528 was verified by animal experiments. Results Higher levels of circ_0003528 were obtained in NSCLC samples and cell lines, and patients with high circ_0003528 expression had a worse prognosis. Silence of circ_0003528 decreased xenograft growth in mouse models and induced cell apoptosis and repressed cell viability, proliferation, invasion, EMT, angiogenesis, and immune escape in NSCLC cells in vitro. Mechanistically, circ_0003528 controlled programmed cell death ligand 1 (PDL1) expression through interaction with miR‐511‐3p. The inhibiting impacts of circ_0003528 knockdown on NSCLC cell malignant transformation and immune escape were weakened after miR‐511‐3p silencing. Moreover, PDL1 overexpression partially counteracted miR‐511‐3p upregulation‐mediated suppression on NSCLC cell malignant transformation and immune escape. Conclusions Circ_0003528 facilitated NSCLC cell malignant transformation and immune escape through regulation of the miR‐511‐3p/PDL1 axis, highlighting the oncogenic role of circ_0003528 in NSCLC.
Previously we showed that aldehyde dehydrogenase 1A1 (ALDH1A1) is a new mediator for resistance of DLBCL to CHOP and a facility predictor of clinical prognosis. In the present study, knockdown and inhibitor of ALDH1A1 were applied to identify the role of ALDH1A1 in Raji cells. CCK-8 and clone formation assay were applied to determine the CHOP sensitivity and clone formation ability. Caspase colorimetric assay and Annexin V/FITC staining was performed to determine the degree of apoptosis. Western blot analysis was used to detect the NF-κB/STAT3 signaling proteins and apoptotic-associated proteins. Real-time quantitative PCR (RT-PCR) was used to identify the differential expression of ALDH1A1 between NHL patients and healthy donors. We demonstrated that inhibition of ALDH1A1 increased the sensitivity of Raji cells to CHOP, as indicated by increased cytotoxicity, reduced clonogenicity, activated caspase-3/-9, decreased NF-κB/STAT3 signaling and increased pro-apoptosis signaling, ad increased apoptosis rate. Moreover, we found high ALDH1A1 expression was associated with poor prognosis in NHL patients. Our data revealed the critical role of ALDH1A1 in NHL and provides a theoretical basis for the use of ALDH1A1 inhibitors in NHL patients.
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