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In this study, we evaluated the physiological effects of fermented metabolites derived from puffed grains (z), fermented using Bacillus amyloliquefaciens NPKE6, a strain isolated from Korean water kimchi. In vitro assays showed that NPKE6-FM significantly increased antioxidant enzyme activities (SOD, CAT, GPx) and digestive enzyme activities (α-amylase, protease), suggesting its strong biofunctional potential. To confirm its in vivo efficacy, we established two inflammatory disease models—ulcerative colitis and liver injury—in male C57BL/6 mice. Colitis was induced by oral administration of 1% dextran sodium sulfate (DSS, 1 mL), while liver injury was induced by intraperitoneal injection of acetaminophen (APAP, 300 mg/kg) three times per week for 4 weeks. In disease-induced control groups, elevated serum biomarkers (AST, ALT, ALP) and reduced antioxidant activity were observed. Experimental groups received 10 or 50 mg/kg/day of NPKE6-FM for 4 weeks. Treatment significantly restored antioxidant enzyme levels and reduced inflammatory markers such as TNF-α and IL-6. In the colitis model, NPKE6-FM alleviated DSS-induced tissue damage, evidenced by improved colon length, weight, and histological scores. Gene expression analysis showed downregulation of iNOS and COX-2 in colon tissues and Akt and MCP-1 in liver, indicating molecular anti-inflammatory effects. Although liver histopathology did not show marked improvement, biochemical and gene expression results supported its protective role. In summary, NPKE6-FM demonstrated potent antioxidant and anti-inflammatory activities in vitro and in vivo, indicating its potential as a functional food additive to prevent or alleviate inflammatory conditions such as colitis and liver injury.

Paclitaxel (Tx) is a widely used therapeutic chemical for breast cancer treatment; however, cancer recurrence remains an obstacle for improved prognosis of cancer patients. In this study, cold atmospheric plasma (CAP) was tested for its potential to overcome the drug resistance. After developing Tx-resistant MCF-7 (MCF-7/TxR) breast cancer cells, CAP was applied to the cells, and its effect on the recovery of drug sensitivity was assessed in both cellular and molecular aspects. Sensitivity to Tx in the MCF-7/TxR cells was restored up to 73% by CAP. A comparison of genome-wide expression profiles between the TxR cells and the CAP-treated cells identified 49 genes that commonly appeared with significant changes. Notably, 20 genes, such as KIF13B, GOLM1, and TLE4, showed opposite expression profiles. The protein expression levels of selected genes, DAGLA and CEACAM1, were recovered to those of their parental cells by CAP. Taken together, CAP inhibited the growth of MCF-7/TxR cancer cells and recovered Tx sensitivity by resetting the expression of multiple drug resistance–related genes. These findings may contribute to extending the application of CAP to the treatment of TxR cancer.

Background: Tamoxifen (tam) is widely used to treat estrogen-positive breast cancer. However, cancer recurrence after chemotherapy remains a major obstacle to achieve good patient prognoses. In this study, we aimed to identify genes responsible for epigenetic regulation of tam resistance in breast cancer. Methods: Methylation microarray data were analyzed to screen highly hypomethylated genes in tam resistant (tamR) breast cancer cells. Quantitative RT-PCR, Western blot analysis, and immunohistochemical staining were used to quantify expression levels of genes in cultured cells and cancer tissues. Effects of matrix metalloproteinase-1 (MMP1) expression on cancer cell growth and drug resistance were examined through colony formation assays and flow cytometry. Xenografted mice were generated to investigate the effects of MMP1 on drug resistance in vivo. Results: MMP1 was found to be hypomethylated and overexpressed in tamR MCF-7 (MCF-7/tamR) cells and in tamR breast cancer tissues. Methylation was found to be inversely associated with MMP1 expression level in breast cancer tissues, and patients with lower MMP1 expression exhibited a better prognosis for survival. Downregulating MMP1 using shRNA induced tam sensitivity in MCF-7/tamR cells along with increased apoptosis. The xenografted MCF-7/tamR cells that stably expressed short hairpin RNA (shRNA) against MMP1 exhibited retarded tumor growth compared to that in cells expressing the control shRNA, which was further suppressed by tam. Conclusions: MMP1 can be upregulated through promoter hypomethylation in tamR breast cancer, functioning as a resistance driver gene. MMP1 can be a potential target to suppress tamR to achieve better prognoses of breast cancer patients.

Ginsenoside Rg3 exerts antiproliferation activity on cancer cells by regulating diverse noncoding RNAs. However, little is known about the role of long noncoding RNAs (lncRNAs) or their relationship with competitive endogenous RNA (ceRNA) in Rg3-treated cancer cells. Here, a lncRNA (ATXN8OS) was found to be downregulated via Rg3-mediated promoter hypermethylation in MCF-7 breast cancer cells. SiRNA-induced downregulation of ATXN8OS decreased cell proliferation but increased apoptosis, suggesting that the noncoding RNA possessed proproliferation activity. An in silico search for potential ATXN8OS-targeting microRNAs (miRs) identified a promising candidate (miR-424-5p) based on its high binding score. As expected, miR-424-5p suppressed proliferation and stimulated apoptosis of the MCF-7 cells. The in silico miR-target-gene prediction identified 200 potential target genes of miR-424-5p, which were subsequently narrowed down to seven that underwent hypermethylation at their promoter by Rg3. Among them, three genes (EYA1, DACH1, and CHRM3) were previously known oncogenes and were proven to be oppositely regulated by ATXN8OS and miR-424-5p. When taken together, Rg3 downregulated ATXN8OS that inhibited the tumor-suppressive miR-424-5p, leading to the downregulation of the oncogenic target genes.

Cold atmospheric plasma (CAP) can induce cancer cell death. The majority of gene regulation studies have been biased towards reactive oxygen species (ROS) among the physicochemical components of CAP. The current study aimed to systemically determine the distribution of target genes regulated by the ROS and non-ROS constituents of CAP. Genome-wide expression data from a public database, which were obtained after treating U937 leukemia and SK-mel-147 melanoma cells with CAP or H2O2, were analyzed, and gene sets regulated by either or both of them were identified. The results showed 252 and 762 genes in H2O2-treated U937 and SK-mel-147 cells, respectively, and 112 and 843 genes in CAP-treated U937 and SK-mel-147 cells, respectively, with expression changes higher than two-fold. Notably, only four and two genes were regulated by H2O2 and CAP in common, respectively, indicating that non-ROS constituents were responsible for the regulation of the majority of CAP-regulated genes. Experiments using ROS and nitrogen oxide synthase (NOS) inhibitors demonstrated the ROS- and reactive nitrogen species (RNS)-independent regulation of PTGER3 and HSPA6 when U937 cancer cells were treated with CAP. Taken together, this study identified CAP-specific genes regulated by constituents other than ROS or RNS and could contribute to the annotation of the target genes of specific constituents in CAP.

Cold atmospheric plasma (CAP) has been recognized as a potential alternative or supplementary cancer treatment tool, which is attributed by its selective antiproliferation effect on cancer cells over normal cells. Standardization of the CAP treatment in terms of biological outputs such as cell growth inhibition and gene expression change is essential for its clinical application. This study aims at identifying genes that show consistent expression profiles at a specific CAP condition, which could be used to monitor whether CAP is an appropriate treatment to biological targets. To do this, genes showing differential expression by two different CAP treatment conditions were screened in the MCF-7 breast cancer cells. As a result, ZNRD1 was identified as a potential marker with being consistently upregulated by 600 s but downregulated by the 10×30 s CAP treatment scheme. Expression of ZNRD1 was increased in breast cancer tissues compared to normal tissues, judged by cancer tissue database analysis, and supported by the antiproliferation after siRNA-induced downregulation in MCF-7. Interestingly, the antisense long noncoding RNA (lncRNA) of ZNRD1, ZNRD1-AS1, was regulated to the opposite direction of ZNRD1 by CAP. The siRNA-based qPCR analysis indicates that ZNRD1 downregulates ZNRD1-AS1, but not vice versa. ZNRD1-AS1 was shown to increase a few cis-genes such as HLA-A, HCG9, and PPP1R11 that were also regulated by CAP. Altogether, this study identified a pair of gene and its antisense lncRNA of which expression is precisely controlled by CAP in a dose-dependent manner. These genes could help elucidate the molecular mechanism how CAP regulates lncRNAs in cancer cells.

Hutchinson–Gilford progeria syndrome, caused by a mutation in the LMNA gene, leads to increased levels of truncated prelamin A, progerin, in the nuclear membrane. The accumulation of progerin results in defective nuclear morphology and is associated with altered expression of linker of the nucleoskeleton and cytoskeleton complex proteins, which are critical for nuclear signal transduction via molecular coupling between the extranuclear cytoskeleton and lamin‐associated nuclear envelope. However, the molecular mechanisms underlying progerin accumulation‐induced nuclear deformation and its effects on intranuclear chromosomal organization remain unclear. Here, the spatiotemporal evolution of nuclear wrinkles is analyzed in response to variations in substrate stiffness using a doxycycline‐inducible progerin expression system. It is found that cytoskeletal tension regulates the onset of progerin‐induced nuclear envelope wrinkling and that the molecular interaction between SUN1 and LMNA controls the actomyosin‐dependent attenuation of nuclear tension. Genome‐wide analysis of chromatin accessibility and gene expression further suggests that an imbalance in force between the intra‐ and extranuclear spaces induces nuclear deformation, which specifically regulates progeria‐associated gene expression via modification of mechanosensitive signaling pathways. The findings highlight the crucial role of nuclear lamin–cytoskeletal connectivity in bridging nuclear mechanotransduction and the biological aging process. The premature aging‐related progerin leads to defective nuclear morphology and is associated with disrupted molecular coupling between the extranuclear cytoskeleton and lamin‐associated nuclear envelope. It is discovered that progerin expression reduces nuclear tension, forms nuclear wrinkling, and enhances chromatin dynamics, thereby regulating progerin‐induced mechanosensitive signaling pathways.

Short-wave infrared (SWIR) detectors and emitters have a high potential value in several fields of applications, including the internet of things (IoT) and advanced driver assistance systems (ADAS), gas sensing. Indium Gallium Arsenide (InGaAs) photodetectors are widely used in the SWIR region of 1–3 μm; however, they only capture a part of the region due to a cut-off wavelength of 1.7 μm. This study presents an InAs p-i-n photodetector grown on a GaAs substrate (001) by inserting 730-nm thick In x Al 1−x As graded and AlAs buffer layers between the InAs layer and the GaAs substrate. At room temperature, the fabricated InAs photodetector operated in an infrared range of approximately 1.5–4 μm and its detectivity ( D * ) was 1.65 × 10 8  cm · Hz 1/2  · W −1 at 3.3 μm. To demonstrate performance, the Sherlock Holmes mapping images were obtained using the photodetector at room temperature.

Nuclear Tension In article number 2502375, Dong‐Hwee Kim, and co‐workers present a mechanobiological mechanism of progerin‐induced wrinkling of nuclear surface. They demonstrate a new biophysical aging process that the abnormal nuclear shape leads to the regulation of aging‐dependent changes of gene profiles.