Retraction of: Diagnostic Value of Exosomal miR-148a-3p in the Serum of Patients with Differentiated Thyroid Cancer.

This retracts the article DOI: 10.7754/Clin.Lab.2020.200519.

Diagnostic Value of Exosomal miR-148a-3p in the Serum of Patients with Differentiated Thyroid Cancer.

BACKGROUND: The current study aims to evaluate the expression and diagnostic value of exosomal miR-148a-3p in the serum of DTC patients. METHODS: Exosomes were isolated from the serum of DTC patients and were identified using a transmission electron microscope. RT-PCR was performed to determine the level of exosomal miR-148a-3p in DTC patients. The possible target gene of miR-148a-3p was determined using dual luciferase reporter assay. ROC analysis was performed to determine the diagnostic value of exosomal miR-148a-3p in DTC patients. RESULTS: We identified a novel exosomal miRNA, exosomal miR-148a-3p, that was significantly decreased in the serum of DTC patients compared with that of benign thyroid tumor patients and healthy controls. Further study showed that exosomal miR-148a-3p was correlated with the malignant characteristics of DTC, including tumor diameter, lymph node metastasis (LNM), and higher TNM staging. Dual luciferase reporter assay indicated that IGF-1 was a target gene of miR-148a-3p. ROC analysis demonstrated that the AUC of exosomal miR-148a-3p was better than TgAb and Tg in DTC patients. More importantly, combined use of exosomal miR-148a-3p, TgAb, and Tg significantly enhanced the sensitivity and specificity, indicating exosomal miR-148a-3p is a sensitive biomarker in DTC patients. CONCLUSIONS: Altogether, reduced exosomal miR-148a-3p was associated with the risk of DTC and may be used as a biomarker for the diagnosis of DTC.

Mulberry anthocyanins improves thyroid cancer progression mainly by inducing apoptosis and autophagy cell death.

Dietary anthocyanin compounds have multiple biological effects, including antioxidant, anti-inflammatory, and anti-atherosclerotic characteristics. The present study evaluated the anti-tumor capacity of mulberry anthocyanins (MA) in thyroid cancer cells. Our data showed that MA suppressed SW1736 and HTh-7 cell proliferation in a time- and dose-dependent manner. Meanwhile, flow cytometry results indicated that MA significantly increased SW1736 and HTh-7 cell apoptosis. We additionally observed that SW1736 and HTh-7 cell autophagy was markedly enhanced after MA treatment. Importantly, anthocyanin-induced cell death was largely abolished by 3-methyladenine (3-MA) or chloroquine diphosphate salt (CQ) treatment, suggesting that MA-induced SW1736 and HTh-7 cell death was partially dependent on autophagy. In addition, activation of protein kinase B (Akt), mammalian target of rapamycin (mTOR), and ribosomal protein S6 (S6) were significantly suppressed by anthocyanin exposure. In summary, MA may serve as an adjunctive therapy for thyroid cancer patients through induction of apoptosis and autophagy-dependent cell death.

Clinical study of radiofrequency ablation combined with TACE in the treatment of breast cancer with liver metastasis.

We studied the clinical effects of percutaneous radiofrequency ablation (RFCA) combined with trans-catheter arterial chemoembolization (TACE) in the treatment of breast cancer with liver metastasis. Eighty-eight patients with a diagnosis of breast cancer with liver metastasis for the first time and patients with liver metastasis after radical mastectomy were consecutively selected. The subjects were divided according to the different treatment methods. They were divided either into the control group of 50 cases or the observation group of 38 cases. Breast cancer patients underwent radical mastectomy with conventional systemic venous chemotherapy. The liver metastasis control group used TACE, while the observation group combined RFCA with TACE. The two groups were followed up for a median time of 20 months, and the clinical effects were compared. The effective rate of the observation group was higher than that of the control group; differences were statistically significant (P<0.05). There was no differences in the incidence of complications between the two groups (P>0.05). The progression free survival, median survival time and survival rate of the observation group were increased; differences were statistically significant (P<0.05). Therefore, RFCA combined with TACE in the treatment of breast cancer with liver metastasis is safe and effective.

Decreased miR-124-3p Expression Prompted Breast Cancer Cell Progression Mainly by Targeting Beclin-1.

BACKGROUND: Recent findings have revealed that abnormal expression of microRNAs (miRNA, miR) contributes to the malignancies of various cancers. Here, we report a novel miRNA that regulates the expression of Beclin-1 in breast cancer cells. METHODS: The expression of miR-124-3p and Beclin-1 was identified in breast cancer tissues and breast cancer cell lines. To explore whether Beclin-1 was the target gene of miR-124-3p, luciferase reporter assay was applied. MIR-124-3p was overexpressed or inhibited with the corresponding mimics or inhibitors. The expression of autophagy-related proteins including Beclin-1 and LC3II were explored by western blot and quantitative real-time PCR. RESULTS: We first demonstrated that miR-124-3p was decreased in breast cancer tissues and breast cancer cells lines. Furthermore, we validated that miR-124-3p could negatively regulate the expression of Beclin-1. Increased miR-124-3p significantly decreased the expression of Beclin-1 and LC3I. Further study showed that overexpres- sion of miR-124-3p could partially reverse 4-hydroxytamoxifen (4-OHT)-induced autophagy in breast cancer cells. CONCLUSIONS: Decreased miR-124-3p expression prompted breast cancer cell progression mainly by enhancing the expression of autophagy related protein, Beclin-1.

[The expression of nicotinamide phosphoribosyl transferase and vascular endothelial growth factor-A in gastric carcinoma and their clinical significance].

OBJECTIVES: To study the expression of nicotinamide phosphoribosyl transferase (Nampt) and vascular endothelial growth factor-A (VEGF-A) in gastric carcinoma and investigate their correlations to clinicopathologic features and prognostic significance. METHODS: The proteins of Nampt and VEGF-A in 68 specimens of gastric carcinoma and 59 specimens normal gastric tissue were detected by immunohistochemistry during January 2000 to December 2004, and the 68 patients were followed up. RESULTS: Nampt protein was detected in the cytoplasm of both tissues, and Nampt in gastric carcinoma (13 ± 5) were significantly higher than that in normal gastric tissue (6 ± 3) (t = 7.46, P < 0.01). The expression of Nampt was correlated to invasive depth (F = 4.693, P = 0.034), lymph node metastasis (F = 4.027, P = 0.049), clinical TNM stage (F = 9.979, P = 0.002), but not to gender, age, tumor location, tumor size, differentiation (P > 0.05). The expression of Nampt is correlated with survival of patients that underwent surgical resection for gastric cancer. The survival rate of patients in negative of Nampt was very higher than that of the positive patients, and its co-expression with VEGF-A showed a trend towards poorer survival. The positive correlation was found between the expression of Nampt and VEGF-A in gastric carcinoma (r = 0.293, P = 0.015). CONCLUSIONS: The expression of Nampt is positively correlated to that of VEGF-A in gastric carcinoma. The correlation between the expression of Nampt and VEGF-A in gastric carcinoma plays an important role cooperatively in carcinogenesis, development and metastasis of gastric carcinoma.

Overexpression of Nampt in gastric cancer and chemopotentiating effects of the Nampt inhibitor FK866 in combination with fluorouracil.

Nicotinamide phosphoribosyltransferase (Nampt), an enzyme involved in the NAD⁺ salvage pathway, is over-expressed and important in the carcinogenesis in several types of cancers. The expression of Nampt and its role in gastric cancer remain largely unknown. In this study, using real-time PCR and Western blotting we found that Nampt was overexpressed at the mRNA and protein levels, respectively, in established gastric cancer cells and human gastric cancer tissues. The specific Nampt inhibitor FK866 repressed gastric cancer cell proliferation, as assessed by MTT assay. Using transwell and soft agar clonogenic assays, we also found that FK866 suppressed gastric cancer cell migration and anchorage-independent growth, respectively. These inhibitory effects of FK866 were accompanied by significantly decreased expression of VEGF, MMP2, MMP9 and NF-κB. As determined by MTT assay and flow cytometry, FK866 also increased the chemo-sensitivity of gastric cancer cells to fluorouracil by greater inhibition of cell proliferation and the induction of apoptosis. Our findings indicate that Nampt may be a new therapeutic target for gastric cancer.

Effects of propranolol in combination with radiation on apoptosis and survival of gastric cancer cells in vitro.

BACKGROUND: The National Comprehensive Cancer Network (NCCN) guidelines recommend radiotherapy as a standard treatment for patients with a high risk of recurrence in gastric cancer. Because gastric cancer demonstrates limited sensitivity to radiotherapy, a radiosensitizer might therefore be useful to enhance the radiosensitivity of patients with advanced gastric carcinoma. In this study, we evaluated if propranolol, a ß-adrenoceptor (ß-AR) antagonist, could enhance radiosensitivity and explored its precise molecular mechanism in gastric cancer cells. METHODS: Human gastric adenocarcinoma cell lines (SGC-7901 and BGC-823) were treated with or without propranolol and exposed to radiation. Cell viability and clonogenic survival assays were performed, and cell apoptosis was evaluated with flow cytometry. In addition, the expression of nuclear factor κB (NF-κB), vascular endothelial growth factor (VEGF), cyclooxygenase 2 (COX-2), and epidermal growth factor receptor (EGFR) were detected by western blot and real-time reverse transcription polymerase chain reaction (PCR). RESULTS: Propranolol combined with radiation decreased cell viability and clonogenic survivability. Furthermore, it also induced apoptosis in both cell lines tested, as determined by Annexin V staining. In addition, treatment with propranolol decreased the level of NF-κB and, subsequently, down-regulated VEGF, COX-2, and EGFR expression. CONCLUSIONS: Taken together, these results suggested that propranolol enhanced the sensitivity of gastric cancer cells to radiation through the inhibition of ß-ARs and the downstream NF-κB-VEGF/EGFR/COX-2 pathway.