Type II cGMP‑dependent protein kinase inhibits the migration, invasion and proliferation of several types of human cancer cells
Authors: Min Wu
Yan Tao
Yongchang Chen
Ji Pang
Yan Wu
Hai Qian
Ying Wang
Journal: Molecular Medicine Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: cGMP; protein kinase; cancer cells; proliferation; migration
Affiliations: Department of Physiology, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu 212013, P.R. China.

Abstract:  Previous studies have indicated that type II cyclic guanosine monophosphate (cGMP)‑dependent protein kinase (PKG II) could inhibit the proliferation and migration of gastric cancer cells. However, the effects of PKG II on the biological functions of other types of cancer cells remain to be elucidated. Therefore, the aim of the present study was to investigate the effects of PKG II on cancer cells derived from various types of human tissues, including A549 lung, HepG2 hepatic, OS‑RC‑2 renal, SW480 colon cancer cells and U251 glioma cells. Cancer cells were infected with adenoviral constructs coding PKG II (Ad‑PKG II) to up‑regulate PKG II expression, and treated with 8‑(4‑chlorophenylthio) (8‑pCPT)‑cGMP to activate the kinase. A Cell Counting kit 8 assay was used to detect cell proliferation. Cell migration was measured using a Transwell assay, whereas a terminal deoxynucleotidyl transferase 2'‑deoxyuridine, 5'‑triphosphate nick‑end labeling assay was used to detect cell apoptosis. A pull‑down assay was used to investigate the activation of Ras‑related C3 botulinum toxin substrate (Rac) 1 and western blotting was used to detect the expression of proteins of interest. The present results demonstrated that EGF (100 ng/ml, 24 h) promoted the proliferation and migration of cancer cells, and it suppressed their apoptosis. In addition, treatment with EGF enhanced the activation of Rac1, and up‑regulated the protein expression of proliferating cell nuclear antigen, matrix metalloproteinase (MMP)2, MMP7 and B‑cell lymphoma (Bcl)‑2, whereas it down‑regulated the expression of Bcl‑2‑associated X protein. Transfection of cancer cells with Ad‑PKG II, and PKG II activation with 8‑pCPT‑cGMP, was identified to counteract the effects triggered by EGF. The present results suggested that PKG II may exert inhibitory effects on the proliferation and migration of various types of cancer cells. 

Retracted: No

PubPeer comments:
 In Figure 6A, cell images in the same field of view are  made full use . ![file] In Figure 3A, the same situation. , 
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 #1 Thank you for your comment. We are working on the problems you pointed out and we will respond to you as soon as possible. , 
 Thank you for your comments. We are working on the problems you pointed out and we will respond to you as soon as possible. , 
 Thank you very much for pointing out the above mistakes of our paper. Due to that five cell lines were applied in the experiment and the massive number of images being processed, we mistakenly reused the pictures of the same group. We are terribly sorry for this very serious oversight of our work. u00a0We have checked the original data and corrected these mistakes. These corrections do not change the results and or the conclusions of this paper. Attached are the revised corrected figures for your reference. We are going to get contact with the editor of Molecular Medicine Reports for the matter of replacing the figures as soon as possible. Many thanks againuff01![file] ![file] , 
 Corrigendum, [14 March 2022] . --------------------------- Subsequently to the publication of this paper, an interested reader drew to the authorsu2019 attention that Figs. 3 (showing how PKG II overexpression inhibits the migration of various types of cancer cells) and 6 (showing representative photomicrographs of apoptotic cells under different experimental conditions at x200 magnification) contained apparently duplicated data panels within the figures. After having examined their original data, the authors have realized that these figures were inadvertently assembled incorrectly; specifically, the data shown in the HepG2-Ad-LacZ+EGF and OS-RC-2-Ad-LacZ+EGF panels in Fig. 3A and the HepG2-Ad-LacZ+cGMP+EGF, OS-RC-2-Ad-PKGII+cGMP+EGF and U251-Ad-PKGII+cGMP+EGF panels in Fig. 6A were selected incorrectly. The corrected versions of Figs. 3 and 6 are shown on the next two pages. Note that these errors did not significantly affect the results or the conclusions reported in this paper, and all the authors agree to this Corrigendum. The authors are grateful to the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this and apologize to the readership for any inconvenience caused. ,