Talin1 knockdown prohibits the proliferation and migration of colorectal cancer cells via the EMT signaling pathway
Authors: Chengkun Qin
Feizhao Jiang
Ling Ji
Xianping Cui
Journal: Oncology Letters (2019)
Discipline: CLINICAL MEDICINE
Keywords: colorectal cancer; epithelial-to-mesenchymal transition; migration; proliferation; talin1.
Affiliations: Department of Hepatobiliary Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China., Department of Colorectal Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.

Abstract:  Colorectal cancer (CRC) is the third most commonly diagnosed cancer and the second highest cause of cancer-associated death worldwide. Talin1 activates integrins, which mediate cell adhesion, proliferation, tumorigenesis and metastasis. The aim of the present study was to determine talin1 expression levels in colorectal cancer (CRC) and investigate the role of talin1 in CRC proliferation and invasion in vitro and in vivo. Talin1 protein expression levels were detected in human CRC and adjacent normal tissues by immunohistochemistry. Talin1 short hairpin RNA and control vectors were designed and stably transfected into HCT116 CRC cells. Cell proliferation was determined by MTT assay. Cell migratory and invasive capabilities were detected by wound-healing and Matrigel invasion assays. The expression of proteins in the epithelial-to-mesenchymal transition signaling pathway was determined by western blotting and reverse transcription-quantitative PCR. The effect of talin1 on tumor growth was explored in vivo using BALB/c nude mice. Immunohistochemical analysis of CRC and adjacent normal tissue revealed that talin1 expression was upregulated in CRC. Talin1 knockdown significantly reduced the proliferation, migration and invasive ability of HCT116 cells compared with the control. Protein levels of phosphorylated STAT3 and vimentin were significantly lower in talin1-knockdown HCT116 cell lines compared with the control, whereas protein levels of E-cadherin were increased. Interleukin-6 mRNA levels were significantly increased in patients' blood samples compared with blood samples from healthy controls, as well as in CRC compared with adjacent normal tissue. In vivo experiments demonstrated that talin1 knockdown reduced CRC tumor growth and weight in nude mice. In conclusion, Talin1 knockdown may prevent the proliferation and migration of CRC cells by downregulating various factors involved in the epithelial-to-mesenchymal transition process, such as phosphorylated STAT3 and vimentin; therefore, talin1 may provide a novel therapeutic target for CRC. 

Retracted: Yes

PubPeer comments:
 While idly Googling images of cancer xenografts - as one does - I couldnu2019t help but notice that two papers shared a panel of excised cancerous objects. The papers have in common that they report reduction of tumour volume. But little else apart from the image of duplicated cancers. Thus, cancers are not the same (breast versus colorectal); experiments are not the same (HCV virus-like particles vis-a-vis Talin-1 knockdown); authors are not the same; medical institutes are not the same; years of publication are not the same. With regards to the latter, the papers were published six years apart. The Springer open access licence for the 2013 paper *u201cpermits unrestricted use, distribution, and reproduction in any medium, **provided the original work is properly cited**.u201d* But was it?  , 
 Retraction, July 27, 2021, found here: https: www.spandidos-publications.com 10.3892 ol.2021.12943  Following the publication of this paper, the authors contacted the office to inform us that they had made errors in the compilation of the tumour images shown in Fig. 4A. Further to the contact we received from these authors, an independent enquiry was conducted in the Editorial office, after which we were able to ascertain that the data in question had appeared in slightly modified form in another publication written by different authors 6 years previously. Owing to the fact that the contentious data in the above article had already been published elsewhere prior to its submission to Oncology Letters, thereby undermining our confidence in the presented data, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory response. The Editor apologizes to the readership for any inconvenience caused. ,