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Lavogina, D.

Publications and source records attributed to Lavogina, D..

4 recordsLinked to original sources

Acute high-dose irradiation of human primary ovarian cells reveals a shift in transcriptomics profile and impairment in cell-cell adhesion

STUDY QUESTIONHow do human cortical (cPOCs) and medullary (mPOCs) primary ovarian cells respond to acute X-ray exposure? SUMMARY ANSWERAcute high-dose X-ray exposure causes a shift in cPOCs and mPOCs transcriptomic profiles and impairs significantly their cell-cell adhesion ability. WHAT IS KNOWN ALREADYRadiotherapy is a leading cancer treatment, due to its effectiveness in targeting malignant cells. However, it can also affect healthy cells, potentially causing organ dysfunction, among which ovaries. When targeted radiotherapy is not feasible, fertility preservation is recommended to avoid premature ovarian insufficiency. In addition, the effects of irradiation on ovarian somatic cells remain poorly understood. STUDY DESIGN, SIZE, DURATIONOvarian tissue was obtained from patients undergoing gender-affirming surgery at Karolinska University Hospital Huddinge, Sweden. The ovarian tissue was separated into cortex and medulla, then individually dissociated into single-cell suspensions using mechanical and enzymatic methods. Monolayer cultures from cPOCs and mPOCs were exposed to a single dose of 10 Gy X-ray irradiation or left unexposed as paired controls. Following irradiation, the cells were cultured at various time-points for further molecular and morphological evaluation. PARTICIPANTS/MATERIALS, SETTING, METHODSOvarian tissue from 8 patients (age 23-36 years) was used. Dissociated cPOCs and mPOCs were cultured to 80% confluence and irradiated with 10 Gy (1.33 Gy/min), with non-irradiated controls. Cellular ATP and mitochondrial activity were assessed, followed by immunofluorescence staining for canonical irradiation-induced effects in cells: DNA damage, apoptosis and cell cycle progression. Bulk RNA-sequencing was performed on controls and irradiated samples. Libraries were prepared using the Illumina Stranded mRNA Prep Ligation protocol and sequenced on Illumina NovaSeq6000 platform. Genes were considered to be differentially expressed under the cut-off of false discovery rate (FDR) < 0.05. Subsequently, affected biological pathway was predicted using all expressed genes ranked by log2 fold change again hallmark gene sets. To further investigate the potential upstream regulators, transcription factor enrichment analysis were performed based on DEGs. To assess changes at protein level, we mapped the proteomic profile using liquid chromatography-tandem mass spectrometry. Peptides were considered to be differentially expressed (DEPs) under the cut-off of p-value < 0.01. Finally, we measured the ability of cPOCs and mPOCs to form 3D aggregates after seeding irradiated and non-irradiated cells on Biosilk scaffolds. MAIN RESULTS AND THE ROLE OF CHANCEFollowing irradiation, ATP levels and mitochondrial activity in cPOCs and mPOCs were comparable to controls, indicating minimal irradiation impact on cell viability and proliferation. Immunofluorescence analysis confirmed the modulation of canonical pathways, such as DNA damage, apoptosis and cell cycle in both cPOCs and mPOCs. Transcriptomic analysis showed that cPOCs and mPOCs at 1 h post-irradiation clustered together with the related 1 h control. However, a shift in transcriptomic profile was observed after 4 h and even more after 24 h post-irradiation in both cPOCs and mPOCs. Gene set enrichment analysis (GSEA) indicated upregulation of the p53 pathway at 4 h and 24 h post-irradiation, alongside downregulation of MYC targets, E2F targets, the G2/M checkpoint and mTORC1 pathway. Gene pattern analysis showed irradiation-dependent trends related to extracellular matrix (ECM) organisation, p53-mediated apoptotic mechanisms and chromosome segregation during the 24 h period following irradiation. Additionally, transcription factor enrichment analysis based on DEGs suggested p53 and MYC as potential upstream regulators. On a proteomic level, DEPs associated with ECM organisation and cytoskeleton formation were detected at 4 and 24 h post-irradiation. Finally, X-ray exposure hindered the cell-cell adhesion ability of both cPOCs and mPOCs, leading to impaired formation of Silk-Ovarioids. LARGE SCALE DATAThe RNA sequencing count matrix is deposited in Gene Expression Omnibus (GEO) with accession number GSE291604. The mass spectrometry proteomics data have been deposited to the ProteomeXchange Consortium via the PRIDE partner repository with the dataset identifier PXD061796. The code used for the analysis can be found at https://github.com/tialiv/X-Ovary. LIMITATIONS, REASONS FOR CAUTIONThe ovarian tissue was obtained from gender-affirming surgery patients who received androgen treatment before removal. Even though unlikely, this hormonal treatment might influence ovarian environment and alter cellular response to irradiation. Additionally, in this study the impact of X-ray exposure was assessed on a monolayer cell model, thus limiting the extrapolation power of our results to ovary in vivo. Lastly, the impact of irradiation was focused on the somatic cell populations that are essential for ovarian function. Further studies are needed to investigate the effects of X-ray exposure on ovarian follicles and their function. WIDER IMPLICATIONS OF THE FINDINGSUnderstanding the roles of MYC, p53 and cell adhesion factors in response to irradiation could guide the development of future ovarian protective strategies. These findings lay the foundation for further studies on ovarian tissue protection and fertility preservation in cancer patients. STUDY FUNDING/COMPETING INTEREST(S)This work was funded by the European Unions HORIZON 2020 research and innovation programme (MATER) under the Marie Skodowska-Curie Actions (grant agreement No: 813707), the Estonian Research Council (grants PRG1076 and PSG608), the Orion Research Foundation sr personal grant, the Research grant from the Center for Innovative Medicine (CIMED) and the Karolinska Institutet Consolidator Grant.

cell biology↗

Proteome changes associated with effect of high-dose single-fractionation radiation on lung adenocarcinoma cell lines

Lung cancer is a leading cause of cancer-related mortality globally, with non-small cell lung cancer (NSCLC) representing 85% of cases. Advances in treatment modalities, including the emergence of antibody-drug conjugates and stereotactic radiation therapy, have improved outcomes. However, the possible synergistic effects of these therapies remain underexplored at the molecular level. This study investigated high-dose radiation-induced proteomic changes in lung adenocarcinoma cell line HCC-44 grown adherently and cell line A549, grown as adherent cells and 3D spheroids. Our hypothesis was that proteins upregulated by 10 Gy irradiation serve as resistance drivers in cancerous cells and can thus represent potential therapeutic targets. The label-free mass spectrometry revealed distinct proteomic responses to 10 Gy irradiation, varying by cell line and culturing conditions. Differentially expressed proteins elevated in the irradiated samples included ephrin type-A receptor 2 (EPHA2) in adherent cells and insulin-like growth factor 2 receptor (IGF2R), tetraspanin 3 (TSPAN3) as well as cathepsin D (CTSD) in spheroids. The validation of these targets was carried out via Western blot, immunofluorescence, viability assay and spheroid formation assay. The functional assays demonstrated that irradiation sensitized A549 cells to EPHA2 and CTSD inhibitors. These findings underscore the potential of integrating radiation and targeted therapies in NSCLC treatment, and highlight EPHA2 as a promising candidate for future therapeutic strategies.

cell biology↗

Phthalate monoesters affect membrane fluidity and cell-cell contacts in endometrial stromal cell lines

Phthalate monoesters have been identified as endocrine disruptors in a variety of models, yet understanding of their exact mechanisms of action and molecular targets in cells remains incomplete. Here, we set to determine whether epidemiologically relevant mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) can affect biological processes by altering cell plasma membrane fluidity or formation of cell-cell contacts. As a model system, we chose endometrial stromal cell lines, one of which was previously used in a transcriptomic study with MEHHP or MEHHP-containing mixtures. A short-term exposure (1 h) of membrane preparations to endocrine disruptors was sufficient to induce changes in membrane fluidity/rigidity, whereas different mixtures showed different effects at various depths of the bilayer. A longer exposure (96 h) affected the ability of cells to form spheroids and highlighted issues with membrane integrity in loosely assembled spheroids. Finally, in spheroids assembled from T-HESC cells, MEHHP interfered with the formation of tight junctions as indicated by the immunostaining of zonula occludens 1 protein. Overall, this study emphasized the need to consider plasma membrane, membrane-bound organelles, and secretory vesicles as possible biological targets of endocrine disruptors and offered an explanation for a multitude of endocrine disruptor roles documented earlier.

pharmacology and toxicology↗

Inhibition of epigenetic and cell cycle-related targets in glioblastoma cell lines: onametostat reduces proliferation and viability in both normoxic and hypoxic conditions

The choice of targeted therapies for treatment of glioblastoma patients is currently limited, and most glioblastoma patients die from the disease recurrence. Thus, systematic studies in simplified model systems are required to pinpoint the choice of targets for further exploration in clinical settings. Here, we report screening of 5 compounds targeting epigenetic writers or erasers and 6 compounds targeting cell cycle-regulating protein kinases against 3 glioblastoma cell lines following incubation under normoxic or hypoxic conditions. The viability assay indicated that PRMT5 inhibitor onametostat was endowed with high potency under both normoxic and hypoxic conditions in both MGMT-positive and MGMT-negative cell lines. In U-251 MG and U-87 MG cells, onametostat also affected the spheroid formation at concentrations lower than the currently used chemotherapeutic drug lomustine. Furthermore, in T98-G cell line, treatment with onametostat led to dramatic changes in the transcriptome profile by inducing the cell cycle arrest, suppressing RNA splicing, and down-regulating several major glioblastoma cell survival pathways. In this way, we confirmed that inhibition of epigenetic targets might represent a viable strategy for glioblastoma treatment even in the case of decreased chemo- and radiation sensitivity, although further studies in clinically more relevant models are required.

cancer biology↗