Oncology Research最新文献

Background: The pTNM staging system is widely recognized as the most effective prognostic indicator for cancer. The latest update of this staging system introduced a new pathological staging system (ypTNM) for patients receiving neoadjuvant chemoradiotherapy (NACRT). However, whether the prognostic value of the ypTNM staging system for rectal cancer is similar to that of the pTNM staging system remains unclear. This study was conducted to compare the ypTNM and pTNM staging systems in terms of their prognostic value for patients with nonmetastatic rectal cancer undergoing proctectomy. Material and Methods: This study was conducted at a large teaching hospital. Between January 2014 and December 2022, 542 patients with rectal cancer were analyzed (median follow-up period, 60 months; range, 6-105 months). Of them, 258 and 284 were included in the pTNM and ypTNM groups, respectively. Inverse probability of treatment weighting (IPTW) was performed to account for the effects of confounders. Cox proportional-hazards regression was performed for the between-group comparison of overall survival (OS). Results: The crude model revealed that OS was similar between the two groups (p = 0.607). After performing IPTW, we found that patients with the same ypTNM- and pTNM-classified stages had similar overall survival (hazard ratio = 1.15; 95% CI = 0.76-1.73; p = 0.5074). Conclusions: For patients with rectal cancer who have received preoperative NACRT, the prognostic value of ypTNM staging appears to be similar to that of pTNM staging, mostly because of the downstaging effect of neoadjuvant chemoradiotherapy.

[This retracts the article DOI: 10.3727/096504017X15024946480113.].

[This retracts the article DOI: 10.3727/096504017X14953948675449.].

[This retracts the article DOI: 10.3727/096504017X15144748428127.].

Objectives: EGFR tyrosine kinase inhibitor (EGFR-TKI) therapies such as erlotinib and gefitinib are approved for the treatment of non-small cell lung cancer (NSCLC). However, the high incidence of acquired resistance to these EGFR-TKIs may preclude their effectiveness. Piperlongumine (PPL), an extract from the long pepper fruit (Piper longum), has been shown to possess anticancer properties. The purpose of the study was to investigate piperlongumine as an anticancer agent and to study a combination treatment approach with EGFR-TKIs against lung cancer cells.

Methods: Anticancer efficacy of PPL, erlotinib (ERL), gefitinib (GEF), and cisplatin (CIS) were investigated in H1299 and H1975 cell lines. Cells were treated with PPL, ERL, GEF, and CIS alone, and in combination, cell viability was determined after 72 h. The mechanism of PPL-induced cytotoxicity was investigated via reactive oxygen species (ROS) induction, and apoptosis induction using acridine orange/ethidium bromide staining and flow cytometry. The effect of treatment on EGFR-mediated oncogenic signaling was investigated by immunoblotting for mitogenic and apoptotic markers.

Results: PPL exhibited a potent cytotoxic effect in H1299 and H1975 cells compared to ERL, GEF, and CIS. Combination treatments of PPL with GEF and ERL showed significant reductions in cancer cells compared to control in both cell lines, which were associated with apoptotic induction, but without significant ROS induction. Compared to control, PPL with GEF significantly increased apoptotic cell death in H1975as confirmed with flow cytometry. Treatment with PPL alone and in combination induced anti-mitogenic and apoptotic responses at the molecular level.

Conclusion: PPL sensitized lung cancer cells to EGFR-TKI and induced potent cytotoxic effects at low concentrations.

Background: Osteosarcoma (OS), recognized as the predominant malignant tumor originating from bones, necessitates an in-depth comprehension of its intrinsic mechanisms to pinpoint novel therapeutic targets and enhance treatment methodologies. The role of fat mass and obesity-associated (FTO) in OS, particularly its correlation with malignant traits, and the fundamental mechanism, remains to be elucidated.

Materials and methods: 1. The FTO expression and survival rate in tumors were analyzed. 2. FTO in OS cell lines was quantified utilizing western blot and PCR. 3. FTO was upregulated and downregulated separately in MG63. 4. The impact of FTO on the proliferation and migration of OS cells was evaluated using CCK-8, colony formation, wound healing, and Transwell assays. 5. The expression of miR-150-5p in OS cells-derived exosomes was identified. 6. The binding of miR-150-5p to FTO was predicted by TargetScan and confirmed by luciferase reporter assay. 7. The impact of exosome miR-150-5p on the proliferation and migration of OS cells was investigated.

Results: The expression of FTO was higher in OS tissues compared to normal tissues correlating with a worse survival rate. Furthermore, the downregulation of FTO significantly impeded the growth and metastasis of OS cells. Additionally, miR-150-5p, which was downregulated in both OS cells and their derived exosomes, was found to bind to the 3'-UTR of FTO through dual luciferase experiments. Exosomal miR-150-5p was found to decrease the expression of FTO and inhibit cell viability.

Conclusions: We identified elevated levels of FTO in OS, which may be attributed to insufficient miR-150-5p levels in both the cells and exosomes. It suggests that the dysregulation of miR-150-5p and its interaction with FTO could potentially promote the development of OS.

[This retracts the article DOI: 10.3727/096504018X15149775533331.].

Background: Papillary thyroid cancer (PTC) is the most prevalent histological type of differentiated thyroid malignancy. Circular RNAs (circRNAs) have been implicated in the pathogenesis and progression of various cancers. circTIAM1 (hsa_circ_0061406) is a novel circRNA with aberrant expression in PTC. However, its functional roles in PTC progression remain to be investigated.

Methods: The expression levels of circTIAM1 in the PTC and the matched para-cancerous tissues were detected by quantitative real-time reverse-transcription PCR (qRT-PCR). The subcellular localization of circTIAM1 was examined by fluorescence in-situ hybridization (FISH). Kaplan-Meier plot was used to analyze the association of clinicopathological features with circTIAM1 expression. Bioinformatics databases were utilized to predict the target miRNAs of circTIAM1 and the downstream target mRNAs. RNA pull-down, RIP assay, and dual-luciferase reporter assay were used to confirm the interactions. Functional experiments, such as CCK-8, EDU staining, and apoptosis assays, as well as in vivo xenograft model were employed to explore the impacts of circTIAM1, miR-338-3p, and LIM/SH3 protein 1 (LASP1) on the malignant phenotype of the PTC cells.

Results: CircTIAM1 was highly expressed in PTC cells. Moreover, circTIAM1 silencing suppressed the proliferation and invasion of PTC cells in vitro and impaired tumorigenesis in vivo. Furthermore, miR-338-3p was verified as a miRNA target of circTIAM1. LASP1 was also identified as a downstream target of miR-338-3p. The anti-tumorigenic effect of miR-338-3p overexpression and the pro-tumorigenic effect of LASP1 was further explored by functional assays, which demonstrated that circTIAM1 modulated the PTC progression through targeting miR-338-3p/LASP1 axis.

Conclusion: The overexpression of circTIAM1 is associated with the malignant progression of PTC. A high level of circTIAM1 promotes the malignancy of PTC cells via the miR-338-3p/LASP1 axis.

[This retracts the article DOI: 10.3727/096504018X15152072098476.].

[This retracts the article DOI: 10.3727/096504017X14878518291077.].