Young-Hwa Chung

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that a pair of data panels (namely, the A549T‑eto/FERO, 1 mM and FERO, 12 h panels) in the cell viability experiments shown in Fig. 1B on p. 1235 were partially overlapping, where the data had apparently been derived from the same original source. After having performed an independent review of the data in the Editorial Office, also in Fig. 1B, another pair of overlapping data panels were identified; moreover, strikingly similar data for the α‑P‑glycoprotein blots had been included in different figures (Figs. 1C and 3B), and there appeared to be a splicing event/break in the continuity of the α‑actin bands shown for the control data in Figs. 1C and 3B that wasn't apparent elsewhere for the proteins of interest shown in these figure parts. Owing to these possible anomalies and the duplications of the data that have been identified in this paper, the Editor of International Journal of Oncology has decided that it should be retracted from the Journal on account of a lack of confidence in the presented data. After having been in contact with the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology 44: 1233‑1242, 2014; DOI: 10.3892/ijo.2014.2297].

Skin tissue is susceptible to oxidative stress-induced senescence provoked by ultraviolet (UV) exposure in our daily lives, resulting in photoaging. Herein, we explore whether N-benzyl-N-methyldecan-1-amine (BMDA) derived from garlic ameliorates UVB-induced photoaging. To address this issue, HaCaT keratinocytes were exposed to UVB irradiation under BMDA treatment. The presence of BMDA substantially reduced UVB-induced ROS levels in a dose-dependent manner. BMDA administration counteracted UVB-induced senescence in the β-galactosidase assay. Treatment with BMDA also rescued UVB-exposed cells (S phase; from 18.3 to 25.8%) from cell cycle arrest, similar to the level observed in untreated normal cells. These findings might support our observation that elevated levels of γ-H2AX, a DNA damage marker, under UVB exposure were reduced following BMDA administration. Additionally, BMDA treatment indirectly reduced UVB-induced melanin synthesis in melanocytes since BMDA failed to inhibit tyrosinase activity, a crucial enzyme in melanin synthesis. The topical application of BMDA on the skin of SKH-1 hairless mice also diminished wrinkle formation, supported by recovered collagen levels and the thickness of the epidermis and dermis, compared to those of UVB-control mice. Finally, the BMDA treatment diminished the expression of inflammatory cytokine transcripts such as TNF-α, IL-1β, IL-4, and IL-6 in the UVB-exposed skin tissues. This finding is further supported by Immunofluorescence microscopy, which showed a decrease in the expression of TNF-α, and IL-1β during BMDA treatment. Altogether, as BMDA mitigates UVB-induced photoaging by reducing ROS production, protecting against DNA damage, and suppressing inflammatory cytokine production, it has been proposed as an effective anti-photoaging molecule.

Following the publication of this article, an interested reader drew to the Editor's attention that a pair of data panels in the cellular images shown in Fig. 1A on p. 2317 appeared to be overlapping, such that data which were intended to show the results from differently performed experiments had appparently been derived from the same original source. Moreover, in Fig. 1C and 5A, there appeared to be discrete splicing events for gel slices featured in these figure parts, and for the immunoblotting experiments shown in Fig. 2B, striking likenesses of certain of the bands appeared in different positions in different gels relative to each other where different experimental conditions were being shown, which seemed difficult to attribute purely to coincidence. After having conducted an internal investigation, the Editor of Molecular Medicine Reports agrees with the reader that there were anomalies associated with the presentation of Figs. 1, 2 and 5. Therefore, on the grounds of a lack of confidence in the presented data, the Editor has decided that the article should be retracted from the publication. Upon contacting the authors, all the authors agreed with the decision to retract this paper, except for Dr Randal Johnston, who was not contactable owing to his retirement several years ago. The Editor apologizes to the readership for any inconvenience caused, and we also thank the reader for bringing this matter to our attention. [Molecular Medicine Reports 11: 2315‑2321, 2015; DOI: 10.3892/mmr.2014.2949].

Given the intricate etiology and pathogenesis of atopic dermatitis (AD), the complete cure of AD remains challenging. This study aimed to investigate if topically applying N-benzyl-N-methyldecan-1-amine (BMDA), derived from garlic, and its derivative [decyl-(4-methoxy-benzyl)-methyl-1-amine] (DMMA) could effectively alleviate AD-like skin lesions in 2,4-dinitrochlorobenzene (DNCB)-treated mice. Administering these compounds to the irritated skin of DNCB-treated mice significantly reduced swelling, rash, and excoriation severity, alongside a corresponding decrease in inflamed epidermis and dermis. Moreover, they inhibited spleen and lymph node enlargement and showed fewer infiltrated mast cells in the epidermis and dermis through toluidine-blue staining. Additionally, they led to a lower IgE titer in mouse sera as determined by ELISA, compared to vehicle treatment. Analyzing skin tissue from the mice revealed decreased transcript levels of inflammatory cytokines (TNF-α, IL-1β, and IL-6), IL-4, iNOS, and COX-2, compared to control mice. Simultaneously, the compounds impeded the activation of inflammation-related signaling molecules such as JNK, p38 MAPK, and NF-κB in the mouse skin. In summary, these findings suggest that BMDA and DMMA hold the potential to be developed as a novel treatment for healing inflammatory AD.

As our previous study revealed that N-benzyl-N-methyldecan-1-amine (BMDA), a new molecule originated from Allium sativum, exhibits anti-neoplastic activities, we herein explored other functions of the compound and its derivative [decyl-(4-methoxy-benzyl)-methyl-amine; DMMA] including anti-inflammatory and anti-oxidative activities. Pretreatment of THP-1 cells with BMDA or DMMA inhibited tumor necrosis factor (TNF)-α and interleukin (IL)-1β production, and blocked c-jun terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), MAPKAP kinase (MK)2 and NF-κΒ inflammatory signaling during LPS stimulation. Rectal treatment with BMDA or DMMA reduced the severity of colitis in 2,4-dinitrobenzenesulfonic acid (DNBS)-treated rat. Consistently, administration of the compounds decreased myeloperoxidase (MPO) activity (representing neutrophil infiltration in colonic mucosa), production of inflammatory mediators such as cytokine-induced neutrophil chemoattractant (CINC)-3 and TNF-α, and activation of JNK and p38 MAPK in the colon tissues. In addition, oral administration of these compounds ameliorated collagen-induced rheumatoid arthritis (RA) in mice. The treatment diminished the levels of inflammatory cytokine transcripts, and protected connective tissues through the expression of anti-oxidation proteins such as nuclear factor erythroid-related factor (Nrf)2 and heme oxygenase (HO)1. Additionally, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels did not differ between the BMDA- or DMMA-treated and control animals, indicating that the compounds do not possess liver toxicity. Taken together, these findings propose that BMDA and DMMA could be used as new drugs for curing inflammatory bowel disease (IBD) and RA.

Chutima Kaewpiboon, Nawong Boonnak, Sirichat Kaowinn, Natpaphan Yawut, Young-Hwa Chung. J Cancer Prev 2022;27:112-21. https://doi.org/10.15430/JCP.2022.27.2.112

Jonggi Choi, Jina Park, Danbi Lee, Ju Hyun Shim, Kang Mo Kim, Young-Suk Lim, Han Chu Lee, and Young-Hwa Chung. Gut and Liver 2022;16:964-75. https://doi.org/10.5009/gnl210416

Natpaphan Yawut, Sirichat Kaowinn, Il-Rae Cho, Phatcharaporn Budluang, Seonghye Kim, Suhkmann Kim, So Eun Youn, Sang Seok Koh & Young-Hwa Chung. BMB Reports 2022;55:98-103. https://doi.org/10.5483/BMBRep.2022.55.2.118

Overexpression of cancer upregulated gene (CUG) 2 induces cancer stem cell-like phenotypes, such as enhanced epithelial-mesenchymal transition, sphere formation, and doxorubicin resistance. However, the precise mechanism of CUG2-induced oncogenesis remains unknown. We evaluated the effects of overexpression of CUG2 on microRNA levels using a microRNA microarray. Levels of miR-3656 were decreased when CUG2 was overexpressed; on the basis of this result, we further examined the target proteins of this microRNA. We focused on Jumonji C domain-containing protein 5 (JMJD5), as it has not been previously reported to be targeted by miR-3656. When CUG2 was overexpressed, JMJD5 expression was upregulated compared to that in control cells. A 3′ untranslated region (UTR) assay revealed that an miR-3656 mimic targeted the JMJD5 3′UTR, but the miR-3656 mimic failed to target a mutant JMJD5 3′UTR, indicating that miR-3656 targets the JMJD5 transcript. Administration of the miR-3656 mimic decreased the protein levels of JMD5 according to Western blotting. Additionally, the miR-3656 mimic decreased CUG2-induced cell migration, evasion, and sphere formation and sensitized the cells to doxorubicin. Suppression of JMJD5, with its small interfering RNA, impeded CUG2-induced cancer stem cell-like phenotypes. Thus, overexpression of CUG2 decreases miR-3656 levels, leading to upregulation of JMJD5, eventually contributing to cancer stem cell-like phenotypes.