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Lan Yu,1 Hui Li,2 Zhiying Li,1 Jianchao Jia,1 Zhouying Wu,1 Min Wang,1 Feng Li,1 Zongqi Feng,1 Huilin Xia,3 Guanxin Gao3 1Clinical Medical Research Center, Inner Mongolia People’s Hospital, Hohhot 010017, People’s Republic of China; 2Department of Oncology, Inner Mongolia People’s Hospital, Hohhot 010017, People’s Republic of China; 3Medical Engineering Department, Inner Mongolia People’s Hospital, Hohhot 010017, People’s Republic of ChinaCorrespondence: Huilin Xia; Guanxin GaoMedical Engineering Department, Inner Mongolia People’s Hospital, No. 20 Zhaowuda Road, Saihan District, Hohhot 010017, People’s Republic of ChinaEmail nmyyxhl@163.com; 840868023@qq.comIntroduction: Long non-coding RNAs (lncRNAs) are regarded as crucial regulators for cancer initiation and progression. Heart and Neural Crest Derivatives Expressed 2 antisense RNA 1 (HAND2-AS1) was recently proposed to function as tumor suppressor in several human cancers. However, its role in gastric cancer (GC) remains unclear.Methods: HAND2-AS1 expression in GC tissues and normal tissues was analyzed at GEPIA(a web server for gene expression profiling analysis). Moreover, RT-qPCR method was utilized to explore HAND2-AS1 expression in GC cells and normal cell. In vitro experiments were carried out using cell counting kit-8 assay, colony formation assay, and flow cytometry assay, respectively. Bioinformatic analysis and luciferase activity reporter assay were performed to identify the downstream targets of HAND2-AS1.Results: We found HAND2-AS1 has decreased expression in both GC tissues and cells. Overexpression of HAND2-AS1 was able to inhibit GC cell proliferation, colony formation, but promote apoptosis. On the contrary, knockdown of HAND2-AS1 could cause the opposite effects on GC cells. Furthermore, HAND2-AS1 was shown tofunction as acompetitive RNA that binds with microRNA-590-3p (miR-590-3p) to affect the expression of potassium sodium-activated channel subfamily T member 2 (KCNT2).Discussion: Our results indicated the tumor suppressive role of HAND2-AS1 in GC. Also, the newly identified HAND2-AS1/miR-590-3p/KCNT2 axis will help us to understand the role of HAND2-AS1 in cancer.Keywords: HAND2-AS1, miR-590-3p, KCNT2, gastric cancer

Qing Liu,1,2,* Hongwei Xia,2,* Sheng Zhou,1,2 Qiulin Tang,1,2 Jitao Zhou,1 Min Ren,1 Feng Bi1,2 1Department of Abdominal Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu 610041, People’s Republic of China; 2Laboratory of Molecular Targeted Therapy in Oncology, West China Hospital, Sichuan University, Chengdu 610041, People’s Republic of China*These authors contributed equally to this workCorrespondence: Feng BiDepartment of Abdominal Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu 610041, People’s Republic of ChinaTel +86 189 8060 1771Email bifeng@scu.edu.cnBackground: Statins, which are used to lower blood cholesterol levels by inhibiting HMG-CoA reductase, have shown anticancer effects in many cancer cells. However, the role of statins in gastric cancer remains unclear. This study aims to investigate whether the statins could antagonize progression of gastric cancer cells and tried to find the molecule mechanism.Methods: Effects of simvastatin on the morphology, proliferation, migration, apoptosis, and invasion of gastric cancer cells were detected and compared. Western blotting, cell viability assay, fluorescence, and transfection were employed to study the molecule mechanism of the effects and the interaction between YAP and β-catenin signaling.Results: Simvastatin could inhibit proliferation, migration and invasion, and promote the apoptosis in gastric cancer cells. Mechanistic studies showed that simvastatin treatment could inhibit the expression of β-catenin and the activity of YAP and the downstream targets of YAP and β-catenin in gastric cancer cells. Moreover, we found that YAP and β-catenin could form a positive feedback loop in gastric cancer cells. Further investigation revealed that simvastatin mainly acted through by inhibiting the activity of RhoA to inhibit YAP and β-catenin, and the geranylgeranyl pyrophosphate pathway mediated this regulation.Conclusion: Statins represent a promising therapeutic option for gastric cancer by simultaneously targeting YAP and β-catenin signaling.Keywords: gastric cancer, simvastatin, YAP, β-catenin, RhoA

Jiabin Liu, 1,* Rui-Xi Hua, 1, 2,* Yun Cheng, 3,* Jinhong Zhu, 1, 4 Jiao Zhang, 5 Jiwen Cheng, 6 Haixia Zhou, 7 Huimin Xia, 1 Jun Bian, 8 Jing He 1 1Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou 510623, Guangdong, People’s Republic of China; 2Department of Oncology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510080, Guangdong, People’s Republic of China; 3Department of Gynecology, Nanjing First Hospital Affiliated to Nanjing Medical University, Nanjing 210006, Jiangsu, People’s Republic of China; 4Department of Clinical Laboratory, Biobank, Harbin Medical University Cancer Hospital, Harbin 150040, Heilongjiang, People’s Republic of China; 5Department of Pediatric Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, People’s Republic of China; 6Department of Pediatric Surgery, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710004, Shaanxi, People’s Republic of China; 7Department of Hematology, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou 325027, Zhejiang, People’s Republic of China; 8Department of General Surgery, Xi’an Children’s Hospital, Xi’an Jiaotong University Affiliated Children’s Hospital, Xi’an 710003, Shaanxi, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jing HeDepartment of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, 9 Jinsui Road, Guangzhou 510623, Guangdong, People’s Republic of ChinaTel/Fax +86-2038076560Email hejing198374@gmail.comJun BianDepartment of General Surgery, Xi’an Children’s Hospital, Xi’an Jiaotong University Affiliated Children’s Hospital, 69 Xiju Court Lane, Xi’an 710003, Shaanxi, People’s Republic of ChinaTel/Fax +86-2987692108Email blandbird@126.comBackground: Neuroblastoma, mainly affecting children, is a lethal malignancy arising from the developing sympathetic nervous system. The genetic etiology of neuroblastoma remains mostly obscure. High mobility group AT-hook 2 (HMGA2), an oncogenic gene, is up-regulated in many tumors. Single nucleotide polymorphisms (SNPs) often modify cancer susceptibility. However, no studies are investigating the association between HMGA2 SNPs and neuroblastoma susceptibility.Methods: We conducted a four-center case-control study to evaluate the association between three HMGA2 polymorphisms (rs6581658 A>G, rs8756 A>C and rs968697 T>C) and neuroblastoma susceptibility in a Chinese population with 505 cases and 1070 controls. Logistic regression was performed to evaluate the strength of the association.Results: We found that the rs8756 AC/CC genotypes were associated with a reduced neuroblastoma risk when compared to rs8756 AA genotype [Adjusted odds ratio (OR)=0.74, 95% confidence interval (CI)=0.56– 0.99, P=0.039]. Carriers with 3 protective genotypes have lower neuroblastoma susceptibility than those without or with 0– 2 protective genotypes. The stratified analysis revealed that the protective effects of rs8756 AC/CC genotypes were more predominant among children of age > 18 months, males, and subgroups with the tumor in the mediastinum. Furthermore, haplotype analysis uncovered that haplotype ACC significantly reduced neuroblastoma risk.Conclusion: Our study indicated HMGA2 rs8756 A>C polymorphism is significantly associated with decreased neuroblastoma risk.Keywords: neuroblastoma, susceptibility, HMGA2, polymorphism

Sheng Zhou,1,2 Meilin Ren,1,2 Huanji Xu,1,2 Hongwei Xia,2 Qiulin Tang,2 Ming Liu1 1Department of Abdominal Oncology, West China Hospital, Sichuan University, Chengdu, Sichuan Province 610041, People’s Republic of China; 2Laboratory of Molecular Targeted Therapy in Oncology, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Collaborative Innovation Center for Biotherapy, Chengdu, Sichuan Province 610041, People’s Republic of ChinaCorrespondence: Qiulin Tang; Ming Liu Tel +86-28-85164045Fax +86-28-85423203Email tangqiulin1981@163.com; mingliu721@aliyun.comBackground: Colon cancer is one of the most common cancers worldwide. IFN-stimulated gene 15 (ISG15), a ubiquitin-like molecule, is strongly up-regulated by type I interferon as a crucial response to a variety of microbial and cellular stress stimuli. However, the role of ISG15 in colon cancer remains unclear.Methods: The expression of ISG15 in colon cancer tissues and cell lines was detected by using Western blotting and immunohistochemistry. ISG15 expression levels of colon cancer cells treated with trametinib was verified by using the data downloaded from the Gene Expression Omnibus (GEO) databases, quantitative real-time PCR analysis and Western blots assays. ISG15-siRNA was used to silence ISG15 in colon cancer cell line to determine the roles of ISG15 in colon cancer cell proliferation.Results: ISG15 was highly expressed in colon cancer tissues and ISG15 upregulation was closely associated with poor prognoses in colon cancer patients. Enhanced ISG15 expression promoted the migration and proliferation of colon cancer cells in vitro, while ISG15 knockdown decreased cell proliferation and metastasis. In addition, we first found that the mRNA and protein expression of ISG15 were up-regulated following trametinib treatment. Further investigation showed that ISG15 knockdown could enhance the anti-cancer effect of trametinib in colon cancer cells.Conclusion: We proposed an interesting possibility that ISG15 may be a prognostic bio-marker, and the combined targeting of ISG15 and MEK might be a promising therapeutic strategy for colon cancer.Keywords: ISG15, MEK, Trametinib, GEO

Chengxiang Yi*,1,2, Yayi He*,3, Haoran Xia*,1, Helin Zhang4, Peng Zhang1 1Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, People’s Republic of China; 2Tongji University School of Medicine, Tongji University, Shanghai 200433, People’s Republic of China; 3Department of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University Medical School Cancer Institute, Tongji University School of Medicine, Shanghai 200433, People’s Republic of China; 4Department of Thoracic Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang City, People’s Republic of China*These authors contributed equally to this workCorrespondence: Peng ZhangDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, No. 507, Zhengmin Road, Yangpu District, Shanghai, People’s Republic of ChinaTel +86 1 351 218 5932Email zhangpeng1121@tongji.edu.cnHelin ZhangDepartment of Thoracic Surgery, Hebei The Second Hospital of Hebei Medical University, No. 53, Huaxi Road, Xinhua District, Shijiazhuang City, People’s Republic of ChinaEmail zhanghelin@hotmail.comAbstract: Postoperative patients have risk recurring, even for completed resected early stage non-small-cell lung cancer (NSCLC). To control the recurrence rate, neoadjuvant and adjuvant therapies have been applied widely in clinical practice; however, neoadjuvant and adjuvant immunotherapy clinical trials on NSCLC are still being explored. In this review, we summarized the research progress and outline the issues need to be solved on adjuvant and neoadjuvant immunotherapies in NSCLC.Keywords: adjuvant immunotherapies, neoadjuvant immunotherapies, immune checkpoint inhibitor, non-small-cell lung cancer, biomarker, liquid biopsy

Ao Lin1,*, Rui-Xi Hua2,*, Jue Tang1,*, Jinhong Zhu3, Ruizhong Zhang1, Haixia Zhou4, Jiao Zhang5, Jiwen Cheng6, Huimin Xia1, Jing He1 1Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou 510623, Guangdong, People’s Republic of China; 2Department of Oncology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, Guangdong, People’s Republic of China; 3Department of Clinical Laboratory, Biobank, Harbin Medical University Cancer Hospital, Harbin 150040, Heilongjiang, People’s Republic of China; 4Department of Hematology, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou 325027, Zhejiang, People’s Republic of China; 5Department of Pediatric Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, People’s Republic of China; 6Department of Pediatric Surgery, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710004, Shaanxi, People’s Republic of China*These authors contributed equally to this workCorrespondence: Huimin Xia; Jing HeDepartment of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangdong Provincial Key Laboratory of Research in Structural Birth Defect Disease, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, 9 Jinsui Road, Guangzhou 510623, Guangdong, People’s Republic of ChinaTel +860 203 807 6001; +860 203 807 6560Fax +860 203 807 6001; +860 203 807 6560Email xia-huimin@foxmail.com;hejing198374@gmail.comBackground: Neuroblastoma is one of the most common extracranial solid pediatric tumors. KRAS plays an important role in regulating cell proliferation, differentiation, and apoptosis. Single nucleotide polymorphisms (SNPs) in KRAS have been shown to modify susceptibility to multiple tumors, but no specific molecular epidemiology study was reported regarding neuroblastoma.Methods: We conducted a four-center case-control study to explore the association between KRAS gene polymorphisms (rs12587 G>T, rs7973450 A>G, rs7312175 G>A) and neuroblastoma susceptibility with 505 Chinese children and 1070 matched controls.Results: We found that rs7973450 A>G was associated with significantly increased neuroblastoma risk [GG vs. AA: adjusted odds ratio (OR)=4.26, 95% confidence interval (CI)=1.28–14.19, P=0.018; GG vs. AA/AG: adjusted OR=4.27, 95% CI=1.28–14.24, P=0.018]. The stratified analysis further demonstrated that rs7973450 GG genotype carriers had a higher risk to develop neuroblastoma in the subgroups of males, tumor originated from the adrenal gland and clinical stages III+IV.Conclusions: Overall, our results suggested that rs7973450 A>G was associated with increased neuroblastoma risk.Keywords: neuroblastoma, KRAS, polymorphism, susceptibility

Yu L, Li H, Li Z, et al. Onco Targets Ther. 2020;13:3187–3196. The Editor and Publisher of OncoTargets and Therapy wish to retract the published article. Concerns were raised over alleged image duplication in Figures 2D and 3D with similar images from an unrelated article, specifically: Figure 2D, panels pcDNA3.1 and pHAND2-AS1 appear to have been duplicated with similar images in Figure 5C from Kang et al, 2019 (https://doi.org/10.2147/OTT.S204004). Figure 3D, panels si-NC and si-HAND2-AS1 appear to have been duplicated with similar images in Figure 5C from Kang et al, 2019 (https://doi.org/10.2147/OTT.S204004). The authors did not respond to our queries and the Editor determined the findings of the study were no longer valid and advised for the article to be retracted. Our decision-making was informed by our policy on publishing ethics and integrity and the COPE guidelines on retraction. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”. This retraction relates to this paper

Xinqi Shi, Huifang Xia, Weiwei Zhang, Guang Li, Ailin Li Department of Radiation Oncology, The First Hospital of China Medical University, Shenyang, Liaoning, China Abstract: When patients with cirrhosis and severe thrombocytopenia suffer malignant tumors, there is usually no effective and feasible treatment method due to the high risk of hemorrhage. Herein, we report a case in which radiotherapy was given to a patient with a strong desire for the treatment. The patient was a 66-year-old man with a 13-year history of cirrhosis and a 10-year history of thrombocytopenia, and was diagnosed with locally advanced rectal cancer (LARC; T4aN1M0, stage IIIB). The platelet count before radiotherapy was 32 × 109/L, and the blood coagulation was normal. The severity of thrombocytopenia increased after 2 Gy × 7 fractions pelvic radiation, with platelet counts dropping to 16 × 109/L. Platelet counts failed to return to pre-therapy levels after supporting therapy including recombinant human interleukin 11 subcutaneous injection and platelet transfusion. Although radiotherapy was discontinued eventually, the data presented here represent a valuable resource that can help inform treatment decisions for tumor patients with cirrhosis and thrombocytopenia. Keywords: rectal cancer, liver cirrhosis, thrombocytopenia, radiotherapy

Zhuorong Zhang,1,2,* Ruizhong Zhang,1,* Jinhong Zhu,3 Fenghua Wang,1 Tianyou Yang,1 Yan Zou,1 Jing He,1 Huimin Xia1,2 1Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, 2Southern Medical University, Guangzhou, Guangdong, 3Molecular Epidemiology Laboratory and Department of Laboratory Medicine, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, People’s Republic of China *These authors contributed equally tothis work Abstract: Neuroblastoma is a common fatal pediatric cancer of the developing sympathetic nervous system, which accounts for ~10% of all pediatric cancer deaths. To investigate genetic risk factors related to neuroblastoma, many genome-wide association studies havebeen performed, and single nucleotide polymorphisms (SNPs) within HACE1 gene have been identified to associate with neuroblastoma risk. However, the association of the HACE1 SNPs with neuroblastoma needs to be validated in Southern Chinese children. We genotyped five SNPs located in the HACE1 gene (rs4336470 C>T, rs9404576 T>G, rs4079063 A>G, rs2499663 T>C, and rs2499667 A>G) in 256 Southern Chinese patients in comparison with 531 ethnically matched healthy controls. Single locus analysis showed no significant association between any of HACE1 SNPs and neuroblastoma risk in Southern Chinese children. However, when all the risk genotypes were combined, we found a borderline significant trend toward an increased neuroblastoma risk with 4–5 risk genotypes (adjusted odds ratio =1.36, 95% confidence interval=0.98–1.89, P=0.065). Moreover, stratified analysis found that carriers of 4–5risk genotypes tended to develop neuroblastoma in the retroperitoneal region and have more aggressive tumors, progressing to advanced clinical stages III/IV, when compared with those of 0–3 risk genotypes. In conclusion, HACE1 gene may have weak effect on neuroblastoma risk in Southern Chinese children. Large well-designed studies are needed to strengthen our findings. Keywords: HACE1, susceptibility, neuroblastoma, GWAS, polymorphism

Wen Fu,1,2,* Zhen-Jian Zhuo,3,* Wei Jia,1,2 Jinhong Zhu,4 Shi-Bo Zhu,1,2 Ze-Feng Lin,1,2 Feng-Hua Wang,1,2 Huimin Xia,1,2 Jing He,1,2 Guo-Chang Liu1,2 1Department of Pediatric Urology, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, 2Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, 3Faculty of Medicine, School of Chinese Medicine, The Chinese University of Hong Kong, Hong Kong, 4Molecular Epidemiology Laboratory, Department of Laboratory Medicine, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, People’s Republic of China *These authors contributed equally to this work Abstract: Wilms’ tumor is one of the most prevalent pediatric malignancies, ranking fourth in childhood cancer worldwide. TP53 is a critical tumor suppressor gene, which encodes a 53kDa protein, p53. The p53 functions to protect against cancer by regulating cell cycle and apoptosis and maintaining DNA integrity. TP53 gene is highly polymorphic. Several TP53 gene polymorphisms have been considered to be associated with cancer risk. Of them, a nonsynonymous polymorphism, Arg72Pro (rs1042522 C>G), has been most extensively studied for the association with cancer risk; however, few studies have investigated its effect on Wilms’ tumor. Because of the central role of p53 in cell cycle control, the TP53 gene Arg72Pro polymorphism is also a good potential candidate predisposition locus for this pediatric cancer. We genotyped this polymorphism in 145 patients and 531 cancer-free controls recruited from Chinese children by Taqman methodology. Overall, our result suggested a lack of association between the TP53 gene Arg72Pro polymorphism and Wilms’ tumor. In the stratified analysis, we found that carriers of CG/GG genotypes had a significantly increased Wilms’ tumor risk in children not older than 18months (adjusted odds ratio =2.04, 95% confidence interval =1.003–4.13, P=0.049) compared with CC genotype carriers. Our study indicated that the TP53 gene Arg72Pro polymorphism may have a weak, age-related effect on Wilms’ tumor risk in Chinese children. These findings need further validations in other populations with larger sample size. Keywords: TP53, polymorphism, Wilms’ tumor, susceptibility

Tao He,1–3,* Tianming Qiu,4,* Xiaodong Wang,5 Hongxing Gui,6 Xilong Wang,2 Qikuan Hu,3,7 Hechun Xia,2 Gaoyang Qi,1,2 Jinsong Wu,4 Hui Ma2 1Clinical Medicine College, Ningxia Medical University, 2Department of Neurosurgery, General Hospital of Ningxia Medical University, 3Ningxia Key Laboratory of Cerebrocranial Diseases, The National Key Laboratory Incubation Base, Yinchuan, 4Department of Neurosurgery, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, 5Department of Radiology, General Hospital of Ningxia Medical University, Yinchuan, People’s Republic of China; 6Department of Neuroscience and Cell Biology, Robert Wood Johnson Medical School of Rutgers University, Piscataway, NJ, USA; 7Department of Physiology, Ningxia Medical University, Yinchuan, People’s Republic of China *These authors contributed equally to this work Objective: This study investigated the correlation between choline/creatine (Cho/Cr) ratios determined by multivoxel proton magnetic resonance spectroscopy (1H-MRS) and the distribution of cancer stem-like cells (CSLCs) in high-grade gliomas. Patients and methods: Sixteen patients with high-grade gliomas were recruited and underwent 1H-MRS examination before surgery to identify distinct tumor regions with variable Cho/Cr ratios. Using intraoperative neuronavigation, tumor tissues were accurately sampled from regions with high and low Cho/Cr ratios within each tumor. The distribution of CSLCs in samples from glioma tissue regions with different Cho/Cr ratios was quantified by neurosphere culture, immunohistochemistry, and Western blot. Results: The mean neurosphere formation rate in tissues with high Cho/Cr ratios was significantly increased compared with that in low Cho/Cr ratio tissues (13.94±5.94 per 100 cells vs 8.04±3.99 per 100 cells, P

Dayue Liu,1,* Haoming Xia,1,* Fang Wang,2 Cui Chen,2 Jianting Long2 1Department of Surgery, Breast Disease Center, 2Department of Medicinal Oncology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, People’s Republic of China *These authors contributed equally tothis work Background: In this study, we investigated the functional correlation between microRNA-210 (miR-210) and gene of F-box protein 31 (FBXO31) in regulating breast cancer.Methods: Dual-luciferase assay and quantitative real-time polymerase chain reaction were used to investigate the binding of miR-210 with FBXO31 and their expression patterns in breast cancer. miR-210 was inhibited in breast cancer T47D and MCF-7 cells to assess its effect on cancer proliferation, cell cycle progression, and migration. FBXO31 was also downregulated in breast cancer cells to examine its effect on miR-210-mediated breast cancer regulation. The interaction between miR-210 and FBXO31 was further investigated by examining the effect of overexpressing miR-210 on FBXO31-induced suppression of breast cancer proliferation.Results: FBXO31 was the downstream target gene of miR-210 in breast cancer. miR-210 and FBXO31 are inversely expressed in breast cancer cell lines. miR-210 downregulation reduced cancer progression, induced cell cycle arrest, and inhibited cancer migration in T47D andMCF-7 cells. Tumor suppression by miR-210 downregulation was reversed by downregulating FBXO31. In FBXO31-overexpressed breast cancer cells, upregulating miR-210 also reversed the tumor-suppressive effect of FBXO31 on breast cancer proliferation.Conclusion: Our work demonstrated that the expression pattern and tumor regulatory functions of miR-210 and FBXO31 are inversely correlated in breast cancer. Keywords: breast cancer, miR-210, FBXO31, cancer proliferation, cancer migration

Xiaomei Mo,1,2,* Fenghua Zhang,2,* Hui Liang,2 Ming Liu,1 Huahui Li,3 Haiping Xia31Key Laboratory of Marine Drugs, Ministry of Education, School of Medicine and Pharmacy, Ocean University of China, 2Qingdao Women and Children Hospital, 3Department of Laboratory Medicine, Qingdao Municipal Hospital, Qingdao, People's Republic of China *These authors contributed equally to this workObjective: To find out the effect of miR-544a on the invasion of lung cancer cells and to explore the underlying molecular mechanisms.Methods: Micro-ribonucleic acid (miRNA) expression in two different invasive lung cancer cell lines 95C (low invasive ability) and 95D (high invasive ability) was analyzed by miRNA microarray and real-time quantitative polymerase chain reaction (PCR); miR-544a mimic was transfected to 95C, and its invasion ability was detected by transwell migration assay; we predicted the candidate miRNA target genes by TargetScan (Whitehead Institute for Biomedical Research, Cambridge, MA, USA) software and verified the target genes by Western blot.Results: The expression of miR-544a was significantly increased in 95D in miRNA microarray and quantitative PCR tests (P