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In lung adenocarcinoma, low lamin A expression in pleural metastatic cells has been proposed as a pejorative factor. miR-9 physiologically inhibits the expression of lamin A in neural cells and seems to be a central actor in the carcinogenesis and the metastatic process in lung cancer. Thus, it could be a good candidate to explain the reduction of lamin A expression in lung adenocarcinoma cells. miR-9 expression was analyzed in 16 pleural effusions containing metastatic cells from lung adenocarcinoma and was significantly reduced in patients from the 'Low lamin A expression' group compared to patients from the 'High lamin A expression' group. Then, carcinoma cells selection by fluorescence-activated cell sorting (FACS) was performed according to epithelial membrane antigen (EMA) expression, reflecting lamin A expression. miR-9 was underexpressed in lamin A- carcinoma cells compared to lamin A+ carcinoma cells in patients from the 'Low lamin A expression' group, whereas there was no difference of miR-9 expression between lamin A+ and lamin A- carcinoma cells in patients from the 'High lamin A expression' group. These results suggest that miR-9 does not regulate lamin A expression in metastatic cells from lung adenocarcinoma. On the contrary, miR-9 expression was shown to be reduced in lamin A-negative carcinoma cells.
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http://dx.doi.org/10.3390/ijms21051599 | DOI Listing |
Nucleic Acids Res
September 2025
Department of Biosciences & Bioengineering, IIT Bombay, Mumbai 400076, India.
Embryonic stem cells (ESCs), which are susceptible to DNA damage, depend on a robust and highly efficient DNA damage response (DDR) mechanism for their survival. However, the implications of physical force-mediated DNA damage on ESC fate remain unclear. We show that stiffness-dependent spreading of mouse ESCs (mESCs) induces DNA damage through nuclear compression, with DNA damage causing differentiation through Lamin A/C.
View Article and Find Full Text PDFInt J Mol Sci
August 2025
Department of Internal Medicine, Institute of Medical Science, Gyeongsang National University Hospital, Gyeongsang National University College of Medicine, 15 Jinju-daero 816 Beon-gil, Jinju 52727, Republic of Korea.
It was reported that polyphenols extracted from Korean L. (pKAL) have higher anticancer effects in oxaliplatin-resistant (OxPt-R) HCT116 cells than in HCT116 cells. In this study, it was tested whether and how AsO enhances anticancer effects of pKAL in HCT116 and HCT116-OxPt-R colorectal cancer cells.
View Article and Find Full Text PDFAging (Albany NY)
August 2025
Department of Neurodevelopmental Disorder Genetics, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Bleomycin is an effective anticancer agent that causes drug-induced interstitial pneumonia (IP). Medical history is a risk factor for adverse effects, particularly a history of IP and age-related fibrosis. Anti-cancer drugs for lung cancer with idiopathic pulmonary fibrosis (IPF) often aggravate pulmonary fibrosis.
View Article and Find Full Text PDFAging (Albany NY)
August 2025
Epigenetics of Aging, Department of Dermatology and Allergy, TUM School of Medicine, Munich Institute of Biomedical Engineering (MIBE), Technical University of Munich (TUM), Garching 85748, Germany.
Hutchinson-Gilford progeria syndrome (HGPS) is a rare and fatal disorder that causes premature aging, affecting approximately one in 4-8 million births. Most cases result from a mutation in the lamin A/C () gene, leading to the production of progerin, an aberrant lamin A variant that disrupts nuclear architecture and alters gene expression, including microRNA (miRNA) deregulation. This study aimed to investigate the molecular mechanisms underlying HGPS and aging using global miRNA sequencing to identify key deregulated miRNAs.
View Article and Find Full Text PDFTransl Oncol
August 2025
Institute of Bioinformatics and Applied Biotechnology (IBAB), Bangalore, India. Electronic address:
Histone Deacetylases inhibitors (HDACi) modulate the acetylation profile of lysines on the histone tails to facilitate DNA accessibility to transcription factors. While the phenotypes caused by HDAC inhibition on cancer cells have been studied extensively, the nuclear geometry and expression signatures modulated by these enzymes have not been well understood.This work attempts to understand the functional implication of HDAC inhibitor treatment (NaB and MS275) on cervical cancer cells.
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