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TRIM-containing 44 aggravates cardiac hypertrophy via TLR4/NOX4-induced ferroptosis
This study explored the role of TRIM44 on pressure overload-induced cardiac hypertrophy in mice. Mice were subjected to aortic banding to establish an adverse cardiac hypertrophy model, followed by the administration of AAV9-TRIM44 or AAV9shTRIM44 to overexpress or knock down TRIM44. Echocardiography was used to assess cardiac function. H9c2 cells were cultured and transfected with either Ad-TRIM44 or TRIM44 siRNA to overexpress or silence TRIM44. Cells were also stimulated with angiotensin II to establish a cardiomyocyte hypertrophy model. Results indicated that TRIM44 was downregulated in mice hearts and cardiomyocytes t...
Source: Journal of Molecular Medicine - April 29, 2023 Category: Molecular Biology Source Type: research

Coexpression of FOXK1 and vimentin promotes EMT, migration, and invasion in gastric cancer cells
We report that FOXK1 synergizes with vimentin to promote GC invasion and metastasis via the induction of epithelial-mesenchymal transition (EMT). We showed that higher expression levels of FOXK1 were significantly associated with GC development. FOXK1 can physically interact with and stabilize vimentin. Moreover, a positive correlation between the expression of FOXK1 and vimentin was found in GC cells. Higher expression levels of these two proteins were significantly associated with differentiation, lymph node metastasis, AJCC stage, and poorer prognosis. Furthermore, the coexpression of FOXK1 and vimentin enhances cell me...
Source: Journal of Molecular Medicine - November 27, 2018 Category: Molecular Biology Source Type: research

Interleukin-23 receptor signaling mediates cancer dormancy and radioresistance in human esophageal squamous carcinoma cells via the Wnt/Notch pathway
In this study, we investigated the effect of extracellular IL-23 in IL-23 receptor-positive (IL-23R+) esophageal squamous cell carcinoma (ESCC) and explored the mechanisms underlying this effect. We analyzed ESCC tumor tissues by immunohistochemical and immunofluorescence staining and found that IL-23, which was highly expressed, co-localized with Oct-4A in IL-23R+ ESCC cells. In addition, IL-23 treatment significantly increased the accumulation of CD133+ cells and activated the Wnt and Notch signaling pathways in CD133−IL-23R+ ESCC cell lines. Consistently, CD133−IL-23R+ cells pretreated with IL-23 showed stronger ant...
Source: Journal of Molecular Medicine - November 27, 2018 Category: Molecular Biology Source Type: research

Bispecific therapeutic aptamers for targeted therapy of cancer: a review on cellular perspective
AbstractAptamers (Aps), as short single-strand nucleic acids, can bind to their corresponding molecular targets with the high affinity and specificity. In comparison with the monoclonal antibodies (mAbs) and peptides, unique physicochemical and biological characteristics of Aps make them excellent targeting agents for different types of cancer molecular markers (CMMs). Much attention has been paid to the Ap-based multifunctional chimeric and therapeutic systems, which provide promising outcomes in the targeted therapy of various formidable diseases, including malignancies. In the Ap-based chimeric systems, a targeting Ap i...
Source: Journal of Molecular Medicine - July 28, 2018 Category: Molecular Biology Source Type: research

Co-targeting PLK1 and mTOR induces synergistic inhibitory effects against esophageal squamous cell carcinoma
In this study, we found that suppression of PLK1 by specific siRNA or inhibitor attenuated mTOR activity in ESCC cells. Phosphorylated S6, a downstream effector of mTOR signaling, was significantly correlated with overexpression of PLK1 in a subset of ESCC. These data suggest that PLK1 activates mTOR signaling in vitro and in vivo. More importantly, the mTOR inhibitor rapamycin synergized with PLK1 inhibitor BI 2536 to inhibit ESCC cell proliferation in culture and in mice. Notably, combined treatment with BI 2536 and rapamycin produced more potent inhibitory effects on the activation of S6 and AKT than either alone. Furth...
Source: Journal of Molecular Medicine - June 29, 2018 Category: Molecular Biology Source Type: research

Sequential combination of docetaxel with a SHP-1 agonist enhanced suppression of p-STAT3 signaling and apoptosis in triple negative breast cancer cells
AbstractTriple negative breast cancer (TNBC) is an aggressive cancer for which prognosis remains poor. Combination therapy is a promising strategy for enhancing treatment efficacy. Blockade of STAT3 signaling may enhance the response of cancer cells to conventional chemotherapeutic agents. Here we used a SHP-1 agonist SC-43 to dephosphorylate STAT3 thereby suppressing oncogenic STAT3 signaling and tested it in combination with docetaxel in TNBC cells. We first analyzed messenger RNA (mRNA) expression of SHP-1 gene (PTPN6) in a public TNBC dataset (TCGA) and found that higher SHP-1 mRNA expression is associated with better ...
Source: Journal of Molecular Medicine - June 4, 2017 Category: Molecular Biology Source Type: research

Estrogen receptor alpha promotes smoking-carcinogen-induced lung carcinogenesis via cytochrome P450 1B1
In this study, we explored the relationship and function of CYP1B1 and ERα in NNK-induced lung tumorigenesis. CYP1B1 and ERα expression was analyzed in human lung cancer tissues and NNK-induced lung tumor of A/J mice. Cell lines NCI-H23 and NCI-H460 were employed to further study the responsible mechanisms using various cellular and molecular approaches. Our in vivo experiments demonstrated that CYP1B1 and ERα were over-expressed at the early stage of NNK-induced lung tumorigenesis. Microarray analysis found that ERα was involved in the extracellular-signal-regulated kinase (ERK)/MAPK pathway. NNK activated RAS/ERK/AP1...
Source: Journal of Molecular Medicine - June 5, 2015 Category: Molecular Biology Source Type: research

SOCS3 methylation in synergy with Reg3A overexpression promotes cell growth in pancreatic cancer
Abstract Pancreatic cancer (PaC) is the fifth leading cause of cancer death in the world, but the molecular mechanisms for its development remain unclear. Regenerating islet-derived protein 3-alpha (Reg3A) has been reported overexpressed in pancreatic inflammation and associated with PaC malignancies, thus believed as a potential target in inflammation-linked pancreatic carcinogenesis. Silencing of suppressor of cytokine signaling SOCS3, a well-known feedback inhibitor of cell proliferation, has been found in many human cancers. Here, we identified that SOCS3 was aberrantly methylated in its CpG island in 3/5 hu...
Source: Journal of Molecular Medicine - November 28, 2014 Category: Molecular Biology Source Type: research

Inactivation of FoxM1 transcription factor contributes to curcumin-induced inhibition of survival, angiogenesis, and chemosensitivity in acute myeloid leukemia cells
In this study, we found that curcumin inhibited cell survival accompanied by induction of G2/M cell cycle arrest and apoptosis in HL60, Kasumi, NB4, and KG1 cells. This was associated with concomitant attenuation of FoxM1 and its downstream genes, such as cyclin B1, cyclin-dependent kinase (CDK) 2, S-phase kinase-associated protein 2, Cdc25B, survivin, Bcl-2, matrix metalloproteinase (MMP)-2, MMP-9, and vascular endothelial growth factor (VEGF), as well as the reduction of the angiogenic effect of AML cells. We also found that specific downregulation of FoxM1 by siRNA prior to curcumin treatment resulted in enhanced cell s...
Source: Journal of Molecular Medicine - September 3, 2014 Category: Molecular Biology Source Type: research