[Retracted] MicroRNA­122 affects cell aggressiveness and apoptosis by targeting PKM2 in human hepatocellular carcinoma.

Following the publication of both the above article and a corrigendum (doi: 10.3892/or.2021.8073) that was concerned with the correction of overlapping data panels in Figs. 6 and 7, it has been drawn to the Editors' attention by a concerned reader that the proposed replacement cell invasion assay shown in the revised version of Fig. 7A, and also flow cytometric data featured in Fig. 5A and C, were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that these contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Oncology Reports, 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 reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 34: 2054­2064, 2015; DOI: 10.3892/or.2015.4175].

[Corrigendum] MicroRNA­122 affects cell aggressiveness and apoptosis by targeting PKM2 in human hepatocellular carcinoma.

Following the publication of the above article, an interested reader drew to the authors' attention that Figs. 6C and 7A apparently contained overlapping panels, suggesting that these data for purportedly different experiments had been derived from the same original source. The wound­healing result for the anti­miR­122+siRNA PKM2 experiment in the lower panel of Fig. 6C and the transwell invasion result for the anti­miR­122+siRNA PKM2 experiment in Fig. 7A were erroneously selected. Accordingly, the authors repeated these assays and were able to confirm that the results were in accordance with the published results. Consequently, the corrected versions of Figs. 6 and 7, containing the replacement data for Figs. 6C and 7A, are shown opposite. It should be emphasized that the inadvertent errors that occurred during the compilation of these figures did not affect the research results or the conclusions of this article. The authors all agree to this Corrigendum, and are grateful to the Editor of Oncology Reports for allowing them to have the opportunity to correct these errors. The authors also apologize to the readership for any inconvenience these errors may have caused. [the original article was published in Oncology Reports 34: 2054­2064, 2015; DOI: 10.3892/or.2015.4175].

MicroRNA-122 affects cell aggressiveness and apoptosis by targeting PKM2 in human hepatocellular carcinoma.

Human hepatocellular carcinoma (HCC) is a highly invasive tumor with frequent distant metastasis, which is the main cause for the poor prognosis. However, the mechanisms for metastasis remain poorly investigated. MicroRNAs (miRNAs) have been implicated in HCC progression. MicroRNA-122 (miR-122) is considered as a tumor suppressor in human cancer. In the present study, miR-122 expression was found to be significantly lower in HCC than the level in normal tumor-adjacent tissues. miR-122 was clearly silenced or downregulated in five HCC cell lines (HepG2, Hep3B, MHCC97H, Huh7 and SMMC-7721) compared with normal hepatocytes (LO2). HCC patients with low expression of miR-122 had a poor 3-year survival. Univariate analysis and multivariate Cox regression analysis indicated that miR-122 is an independent prognostic factor in HCC. Downregulation of miR-122 promoted proliferation and inhibited apoptosis in Hep3B cells. We found that the public miRNA database (TargetScan) predicted that PKM2 may be a target for miR-122, and the 3'-untranslated region (3'-UTR) of PKM2 contains a highly conserved binding site for miR-122. To identify this, pre-miR-122/anti-miR-122 were respectively transfected into the Hep3B cell line. We found that miR-122 overexpression significantly reduced the level of PKM2. Moreover, knockdown of PKM2 significantly increased miR-122 inhibitor-mediated Hep3B cell apoptosis and reduced miR-122 inhibitor-mediated Hep3B cell migration and invasion. Moreover, re-expression of PKM2 partially abrogated miR-122-induced HCC cell growth arrest and apoptosis in vivo. In conclusion, miR-122 serves as a prognostic biomarker and induces apoptosis and growth arrest by downregulating PKM2 in HCC.

A case of endoscopic ultrasound diagnosis of gastric amyloidosis.

A 37-year-old female presented to our hospital with the complaint of abdominal distension for one month. A gastroscopy examination showed extensive chyme retention and varying erosion and ulceration of the gastric body. The pathology showed moderate chronic inflammation and erosion of the gastric body mucosa, with accompanying Helicobacter pylori infection. She accepted treatment for one month. The patient then accepted to undergo endoscopic ultrasonography, which showed that normal structure of the gastric body intumescence was discernible. The pathology showed chronic mild-moderate inflammation of the gastric body mucosa associated with interstitial amyloidosis, with accompanying Helicobacter pylori infection. She accepted treatment for the eradication of Helicobacter pylori, and the original ulcer healed.