Erratum: [Corrigendum] Chloroquine potentiates the anticancer effect of sunitinib on renal cell carcinoma by inhibiting autophagy and inducing apoptosis.

[This corrects the article DOI: 10.3892/ol.2017.7635.].

Chloroquine potentiates the anticancer effect of sunitinib on renal cell carcinoma by inhibiting autophagy and inducing apoptosis.

Sunitinib based adjuvant chemotherapy combined with chloroquine (CQ) for the treatment of renal cell carcinoma (RCC) is in clinical trials; however, its anti-RCC effect and the mechanism remain unclear. In the present study, the anti-RCC effect of sunitinib with CQ and the underlying mechanism was investigated. An MTT assay demonstrated that CQ enhanced the proliferation inhibitory effect of sunitinib against the OS-RC-2 RCC cell line. CQ inhibited sunitinib-induced autophagy in OS-RC-2, which was evidenced by the inhibition of autophagic vacuoles, acidic vesicular organelle formation, light chain 3 (LC3)-II recruitment to the autophagosomes and the conversion of LC3-I to LC3-II, as induced by sunitinib. The inhibition of autophagy by CQ enhanced sunitinib-induced apoptosis, which was characterized by the activation of caspase-3, caspase-9, Bcl-2 and p53. Additionally, the exposure of OS-RC-2 cells to CQ and sunitinib resulted in the inhibition of AKT, tuberous sclerosis complex 2, mechanistic target of rapamycin and p70 ribosomal S6 kinase, which are associated with cell proliferation. In in vivo study, a combination of sunitinib with CQ in mice significantly reduced OS-RC-2 cell xenograft growth compared with the sunitinib alone group. In conclusion, the present study demonstrated that CQ may enhance the anti-RCC effect of sunitinib by inhibiting the autophagy induced by sunitinib, and enhance the rate of apoptosis. Inhibiting cell proliferation may also serve a role in the synergistic antitumor effect of sunitinib and CQ. These data suggest that combination therapy of sunitinib with CQ may be a promising strategy for adjuvant chemotherapy in RCC.

The expression of microRNA-324-3p as a tumor suppressor in nasopharyngeal carcinoma and its clinical significance.

OBJECTIVE: This study aimed to determine the expression, clinical significance, and possible biologic function of microRNA-324-3p in nasopharyngeal carcinoma (NPC) tissues. METHODS: In total, 54 NPC and 35 control tissues were collected. The correlation between miR-324-3p expression and the clinicopathologic characteristics was analyzed. A dual-luciferase reporter gene assay was employed to examine the predicted target gene of miR-324-3p. The miR-324-3p expression level in 5-8F cells was determined with quantitative reverse transcription-polymerase chain reaction following the transfection of miR-324-3p mimics and inhibitors. Cell proliferation and the percentage of apoptosis were measured with MTT and flow cytometry. Cell invasion ability was assessed by Transwell invasion assay. RESULTS: Our results showed that miR-324-3p was downregulated in the NPC tissues. The expression level of miR-324-3p in poorly differentiated NPC was significantly reduced in comparison with that in well/moderately differentiated NPC. The expression level in clinical stages III/IV was lower than that in clinical stages I/II. Moreover, the expression level of miR-324-3p was significantly lower in NPC patients with lymph node metastasis than that in NPC patients without lymph node metastasis. NPC patients with higher levels of miR-324-3p expression also demonstrated a longer survival time. Predictions from bioinformatics indicated the Hedgehog pathway transcription gene GLI3 as the target gene of miR-324-3p, and the dual- luciferase reporter assay showed that miR-324-3p is directly combined with the 3'-untranslated region of GLI3. The overexpression of miR-324-3p suppressed cell proliferation and invasion, and it enhanced apoptosis in 5-8F cells. CONCLUSION: miR-324-3p can act as a tumor suppressor in NPC cells by the negative regula- tion of GLI3 gene.

Inhibition of Cell Survival by Curcumin Is Associated with Downregulation of Cell Division Cycle 20 (Cdc20) in Pancreatic Cancer Cells.

Pancreatic cancer is one of the most aggressive human tumors in the United States. Curcumin, a polyphenol derived from the Curcuma longa plant, has been reported to exert its antitumor activity in pancreatic cancer. However, the molecular mechanisms of curcumin-mediated tumor suppressive function have not been fully elucidated. In the current study, we explore whether curcumin exhibits its anti-cancer function through inhibition of oncoprotein cell division cycle 20 (Cdc20) in pancreatic cancer cells. We found that curcumin inhibited cell growth, enhanced apoptosis, induced cell cycle arrest and retarded cell invasion in pancreatic cancer cells. Moreover, we observed that curcumin significantly inhibited the expression of Cdc20 in pancreatic cancer cells. Furthermore, our results demonstrated that overexpression of Cdc20 enhanced cell proliferation and invasion, and abrogated the cytotoxic effects induced by curcumin in pancreatic cancer cells. Consistently, downregulation of Cdc20 promoted curcumin-mediated anti-tumor activity. Therefore, our findings indicated that inhibition of Cdc20 by curcumin could be useful for the treatment of pancreatic cancer patients.

MicroRNA-18a as a promising biomarker for cancer detection: a meta-analysis.

Patients with cancer discovered at an early stage have relatively high survival rates. Increasing researches have shown the potential of detecting dysregulated microRNA-18a (miR-18a) to diagnose cancer. However, non-uniform results in previous studies were found. Thus, this meta-analysis was conducted to further explore the clinical applicability of miR-18a as an ideal biomarker for cancer detection. Suitable articles were obtained from online databases like PubMed, Embase, Cochrane, CBM and Wanfang. The Quality Assessment of Diagnostic Accuracy Studies-2 (QUADAS-2) tool was used to evaluate the quality of our meta-analysis. The pooled diagnostic parameters like specificity, sensitivity, diagnostic odds ratio (DOR), positive and negative likelihood ratios (PLR and NLR) and area under the summary receiver operator characteristic curve (SROC) were pooled to assess the entire test accuracy. Overall, 10 studies from 9 articles, including 979 patients with cancer and 713 healthy controls were involved in our meta-analysis. The pooled sensitivity was 0.78 (95% CI: 0.70-0.84) and the corresponding specificity was 0.82 (95% CI: 0.73-0.89). The merged PLR was 4.3 (95% CI: 2.8-6.8), NLR was 0.27 (95% CI: 0.20-0.37), and DOR was 16 (95% CI: 8-31). The pooled AUC was 0.86 (95% CI: 0.83-0.89). Our meta-analysis suggested that miR-18a might open up a new field for novel clinical cancer screening with the merits of high accuracy, non-invasiveness, convenience and cheap cost. However, more reliable studies in larger cohort should be conducted before it is used.

Primary precursor B cell lymphoblastic lymphoma of uterine corpus: case report and review of the literature.

INTRODUCTION: Primary lymphomas of the female genital tract are rare. Most involve the cervix rather than the uterine corpus. Many cases of primary endometrial lymphoma are diagnosed as diffuse large B cell type, whereas the precursor B cell lymphoblastic type is extremely rare. MATERIALS AND METHODS: We report a case of precursor B cell lymphoblastic lymphoma of uterine corpus which was successfully treated with surgery and chemotherapy. Staging evaluation revealed tumor limited to the uterine corpus (stage I(E)). After receiving a total abdominal hysterectomy, bilateral salpingooophorectomy, lymph node dissection and combination chemotherapy, the patient is currently free of disease after follow-up of 42 months. CONCLUSION: If correct diagnosis is established and appropriate therapy is chosen, the prognosis of precursor B-LBL of uterine corpus is expected to be good. The literature on primary precursor B cell lymphoblastic lymphoma of the uterine corpus is reviewed.