With the increasing incidence of papillary thyroid cancer (PTC), more attention has been paid to exploring the mechanism of PTC initiation and progression. In addition, ectopic expression of long noncoding RNAs (lncRNAs) is reported to play a pivotal role in multiple human cancers. Based on these findings, we examined lncRNA ABHD11 antisense RNA 1 (ABHD11-AS1) expression and its clinical significance, biological function and mechanism in PTC. First, we analyzed thyroid ABHD11-AS1 expression in The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Then, qRT-PCR was applied to detect the expression in paired PTC tissues and adjacent normal tissues, as well as in PTC cell lines (TPC-1 and K-1) and a normal thyroid follicular epithelium cell line (Nthy-ori3-1). In addition, we validated the relationship between ABHD11-AS1 expression and clinicopathological features by the Pearson X 2 test. The oncogenic role of ABHD11-AS1 and its regulation of miR-199a-5p in PTC were examined by biological assays. Finally, bioinformatics analysis and mechanism assays were used to elucidate the underlying mechanism. We found that ABHD11-AS1 was remarkably overexpressed in PTC, and high expression was related to tumor size, lymph node metastasis, extrathyroidal extension and advanced TNM stage. Moreover, ABHD11-AS1 enhanced the abilities of cell proliferation, migration, and invasion, inhibited apoptosis in vitro, promoted tumorigenesis in vivo via sponging miR-199a-5p and then induced SLC1A5 activation. In addition, rescue assays were performed to confirm the ABHD11-AS1/miR-199a-5p/SLC1A5 axis. Taken together, the data show that ABHD11-AS1 acts as a competing endogenous RNA (ceRNA) to exert malignant properties in PTC through the miR-199a-5p/SLC1A5 axis. Therefore, our study may shed light on PTC diagnosis and therapies.
OBJECTIVES We investigated the impact of level 4 (L4) lymph node dissection (LND) on overall survival (OS) in left-side resectable non-small-cell lung cancer (NSCLC), with the aim of guiding lymphadenectomy. METHODS A total of 1929 patients with left-side NSCLC who underwent R0 resection between 2001 and 2014 were included in the study. The patients were divided into a group with L4 LND (L4 LND+) and a group without L4 LND (L4 LND−). Propensity score matching was applied to minimize selection bias. The Kaplan–Meier method and Cox proportional hazards model were used to assess the impact of L4 LND on OS. RESULTS A total of 317 pairs were matched. Of the cohort of patients, 20.3% (391/1929) had L4 LND. Of these patients, 11.8% (46/391) presented with L4 lymph node metastasis. L4 lymph node metastasis was not associated with the primary tumour lobes (P = 0.61). Before propensity score matching, the 5-year OS was comparable between the L4 LND+ and L4 LND− groups (69.0% vs 65.2%, P = 0.091). However, after propensity score matching, the 5-year OS of the L4 LND+ group was much improved compared to that of the L4 LND− group (72.9% vs 62.3%, P = 0.002) and L4 LND was an independent factor favouring OS (hazard ratio 0.678, 95% confidence interval 0.513–0.897; P = 0.006). Subgroup analysis suggested that L4 LND was an independent factor favouring OS in left upper lobe tumours. CONCLUSIONS In patients with left-side operable NSCLC, L4 lymph node metastasis was not rare and L4 LND should be routinely performed.
BackgroundThyroid cancer is the most common endocrine malignancy, papillary thyroid carcinoma (PTC) is the main form of thyroid cancer. The long non-coding RNA (lncRNA) zinc finger antisense 1 (ZFAS1) is highly expressed in various cancer tissues and it has been shown to function as a tumor promoter in various cellular processes. However, the role of ZFAS1 in PTC is not well understood currently. Thus, this study aimed to explore the potential roles of ZFAS1 in the development and progression of PTC.Material and methodsPTC tissues (n=80) and noncancerous tissues were collected. Gain- and loss-of-function assays were performed to determine the effect of ZFAS1 on proliferation in K-1 and TPC-1 cells. The ZFAS1/mir-590-3P/HMGA2 aixs were analysed in PTC cell lines.ResultsWe found that the expression of ZFAS1 was increased in PTC tissues and four PTC cell lines (B-CPAP, IHH-4, TPC-1, and K-1). The gain- and loss-of-function assays showed that overexpressing ZFAS1 promoted cell proliferation and inhibited cell apoptosis in PTC cells in vitro. We demonstrated that knockdown of ZFAS1 inhibits tumor growth and upregulation of ZFAS1 promotes tumor growth in vivo. Bioinformatics analysis revealed that miR-590-3p targeted the 3ʹ-UTR of ZFAS1. The double luciferase reporter and RNA-binding protein immunoprecipitation assay demonstrated that miR-590-3p is a target of ZFAS1. Rescue experiments confirmed that miR-590-3p could reverse the effect of ZFAS1 on PTC cells. Moreover, we identified high mobility group AT-hook 2 (HMGA2) to be a downstream target of miR-590-3p and ZFAS1 which activates HMGA2 expression by sponging to miR-590-3p.ConclusionHigh ZFAS1 expression level was associated with the progression of PTC, and ZFAS1 contributed to PTC progression via miR-590-3p/HMGA2 regulatory aixs. Therefore, ZFAS1 might be a potential therapeutic target for PTC intervention.
TAP may be a novel biomarker for PTC and be useful in the adjuvant diagnosis of PTC.
With the improvement of diagnostic technology, the incidence of thyroid cancer (TC) is on the rise. Papillary thyroid carcinoma (PTC) is the most common pathological type of thyroid cancer, therefore, it is important to explore some valuable molecular targets to improve the treatment and prognosis of PTC. Studies have shown that family with sequence similarity 84, member A (FAM84A) is involved in the development of various tumors. However, the role of FAM84A in PTC remains unknown. Herein, we explored the biological function and specific molecular mechanism of FAM84A in PTC. Results indicated that FAM84A was upregulated in PTC tissues and cells. In addition, patients with higher FAM84A expression tended to possess larger tumor size, higher lymph node metastasis rate and advanced TNM stage. Further studies indicated that downregulation of FAM84A could inhibit the development of PTC in vitro and in vivo by repressing the epithelial-mesenchymal transition (EMT) and Wnt/β-catenin signaling pathway. Moreover,
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