Talen-mediated girdin knockout downregulates cell proliferation, migration and invasion in human esophageal carcinoma ECA109 cells
Authors: Wenting Jiang
Qiong Zou
Jianda Zhou
Sheng Xiao
Ke Cao
Peiguo Cao
Chenghui Huang
Journal: Molecular Medicine Reports (2014)
Discipline: CLINICAL MEDICINE
Keywords: Girdin; cell migration; invasion; metastasis; esophageal squamous cell carcinomas (ESCCs)
Affiliations: Department of Oncology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, 410013, P.R. China., Department of Pathology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, 410013, P.R. China., Department of Plastic Surgery, The Third Xiangya Hospital, Central South University, Changsha, Hunan, 410013, P.R. China.

Abstract:  Girdin is an actin-binding Akt substrate that is involved in the regulation of cell migration. Accumulating evidence has revealed that girdin has regulatory effects on invasion and metastasis in several types of cancer. However, the role of girdin in esophageal squamous cell carcinomas (ESCCs) is yet to be investigated. In the present study, tissue microarray data revealed that among 95 cases of ESCC, 27 cases (28.7%) exhibited a low expression of girdin, while 67 cases (71.3%) had an enhanced expression of girdin. However, among 78 cases of adjacent tissues, 64 cases (82.1%) did not express girdin and 14 cases (17.9%) exhibited a low expression of girdin. Furthermore, the expression of girdin was significantly associated with the tumor stage, lymph node metastasis stage, and tumor, lymph node and metastasis stage. Of note, the mean survival time of girdin-positive cases was only 30.62±2.99 months, while it was 53.37±5.02 months in girdin-negative cases, indicating that girdin protein expression is an independent prognostic factor of poor survival. Talen-mediated girdin knockout (KO) significantly suppressed cellular proliferation, migration and invasion in ESCC ECA109 cells. In conclusion, the present study suggested that girdin protein expression was significantly correlated with cancer progression and poor prognosis in ESCCs, and that girdin had a positive role in the regulation of cell proliferation, migration and invasion in ESCC cells. Therefore, girdin may be a potential candidate for the development of novel prognostic tools and therapeutic strategies for ESCCs. 

Retracted: Yes

PubPeer comments:
 Fig 6.  Figure 6. Cell invasion assay data revealed that talen-mediated girdin KO notably suppressed cell invasion in ECA109 cells. ![file] Left-hand and right-hand panels (Control and Girdin-KO) overlap. However, there are differences within the overlapping area, as if cells have been added to one or the other. Here dramatised by superimposing Girdin-KO (after a black white reversal) upon Control: cells unique to Control and to Girdin-KO are black and white respectively; other areas cancel out. ![file] Other versions of the same panel feature, variously identified, in at least a dozen other papers by different authors. E.g. Fig 3 C D from [Zhang et al (2016)] .  Transwell assay were performed to examine the migratory and invasive capacities of Saos-2 and U2OS cells transfected with miR-205 mimic or miR-negative control (NC) mimic , and Fig 7C D,  Transwell assay were performed to examine cell migration and invasion of MG63 or U2OS cells transfected with miR-205 mimic, or co-transfected with miR-205 mimic and RUNX2 plasmid . ![] Also *[above]* Fig 4C from [Lai, Chen Li (2015)] .  a Transwell assay were performed to examine the cell proliferation of AGS cells transfected with miR-133a mimics, miR-133a inhibitor, or co-transfected with miR-133a mimics and FSCN1 plasmid. Control: AGS cells without any transfection. *[below]* Figs 3(B), 6(B) from [Shi et al (2015)] .  Transwell assay was performed to determine the invasive capacity of the Saos-2 and U-2 OS cells transfected with NC scramble miRNA or miR-204 mimics, respectively. Control, Saos-2 and U-2 OS cells without any transfection ...  Transwell assay was performed to determine the invasive capacity of the Saos-2 and U-2 OS cells transfected with Sirt1 siRNA or co-transfected with miR-204 mimics and the Sirt1 plasmid, respectively. Control, Saos-2 and U-2 OS cells without any transfection . ![file] , 
 Retracted [23 July 2021] . -------------------------------------------- Following the publication of this paper, it was drawn to the Editorsu2019 attention by a concerned reader that the Transwell cell migration data shown in Fig. 6 were strikingly similar to data appearing in different form in other articles by different authors; furthermore, there were other possible anomalies associated with these data. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. ,