HOXA10 promotes the development of bladder cancer through regulating FOSL1
Authors: M Xie
W-F Li
Y-P Cui
Z-Y Zhang
W-X Pan
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: HOXA10; bladder cancer; FOSL1; expression characteristics; metastasis
Affiliations: Department of Urology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China. .

Abstract:  Objective: This study was aimed to investigate the expression characteristics of HOXA10 in bladder cancer (BCa), and to further study whether it can promote the development of BCa via regulating FOSL1. Patients and methods: The expression of HOXA10 was examined by quantitative Real Time-PCR (qRT-PCR) in 37 pairs of tumor tissue and paracancerous specimens of BCa patients; meanwhile, in BCa cell lines, the expression of HOXA10 was also verified using qRT-PCR. Subsequently, after HOXA10 knockdown model was constructed in BCa cell lines (EJ and J82) using lentivirus transfection, transwell, as well as wound healing assays, were performed to analyze the influence of the downregulation of HOXA10 on the biological function of BCa cells. Finally, Luciferase reporting assay and cell reverse experiment were applied to explore the specific interaction between HOXA10 and FOSL1. Results: The results of qRT-PCR indicated that the expression level of HOXA10 in BCa tissue samples was remarkably higher than that in adjacent normal ones, with a statistically significant difference. At the same time, the overall survival rate of patients with high expression of HOXA10 was found to be lower than those with low expression. Meanwhile, compared with cells in sh-NC group, the metastasis ability of BCa cells in sh-HOXA10 group was remarkably weakened. In addition, it was found that the levels of FOSL1 and HOXA10 were negatively correlated in BCa tissues. The result of the Luciferase reporter gene assay revealed that HOXA10 could be targeted by FOSL1 through certain binding sites between them. In addition, HOXA10 was found to be capable of further regulating the malignant progression of BCa by modulating FOSL1. Conclusions: HOXA10 expression is remarkably elevated in BCa tissues and cell lines, which is closely relevant to the poor prognosis of BCa patients. In addition, HOXA10 may be able to accelerate BCa metastasis via modulating FOSL1 expression. 

Retracted: No

PubPeer comments:
 *[left]* Fig 3D from [Yu et al (2019)] .  There was a significant negative correlation between the expression levels of SAMD12-AS1 and P53 in glioma tissues. *[right]* Fig 3C from [Liu et al (2019)] .  A significant negative correlation was found between microRNA-106a expression and DAX-1 expression in BC tissues. Please admire the implausible number of points shared between the two scatterplots. ![file] ------------------------------------------------ Afterthought: Here s an even better match with *[right]* Fig 3C from [Pan et al (2019)] .  Significant negative correlation was found between miRNA-374b and EGFR expression levels . ![file] There are so many papers in this *oeuvre* that it s hard to keep up. , 
 From Results:  Knockout of SAMD12-AS1 Inhibited Glioma Progression In Vivo To better explore the role of SAMD12-AS1 in vivo, the transfected T98-G cell line was inoculated in situ into each nude mouse and injected in the left axilla. As shown in Figure 4A and 4B, the tumor volume of nude mice inoculated with the SAMD12-AS1 knockdown vector was reduced. The Methods section never mentions or describes in-vivo experiments on mice. , 
  According to the statistics of the American Brain Tumor Registry (CBTRUS), glioma accounts for 28% of all central nervous system tumors and 80% of intracranial malignant tumors1,2 . Here Ref [2] is  Niu H, Li X, Yang A, Jin Z, Wang X, Wang Q, Yu C, Wei Z, Dou C. Cycloartenol exerts anti-proliferative effects on glioma U87 cells via induction of cell cycle arrest and p38 MAPK-mediated apoptosis. J BUON 2018; 23: 1840-1845 . That paper has [its own PubPeer thread] . It does not support the claims for glioma frequency, and I can see no reason to cite it, unless it was a product of the same papermill.  Currently, the exposure to high dose of ionizing radiation and mutation of high penetrability gene related to rare syndrome have been identified as two risk factors for glioma5,6 . Here Ref [5] is  Ren D, Yang C, Liu N, Wang Z, Wang X, Johnson M, Wang W, Zhang P, Yang H, Liu H, Cheng Y, Wang L, Tu Y. Gene expression profile analysis of U251 glioma cells with shRNA-mediated SOX9 knockdown. J BUON 2018; 23: 1136-1148. [That paper] does not address risk factors for glioma. Are the actual authors given a quota of J.BUOn papers to cite? ,