Reconstitution of pluripotency from mouse fibroblast through Sall4 overexpression.

Somatic cells can be reprogrammed into pluripotent stem cells (iPSCs) by overexpressing defined transcription factors. Specifically, overexpression of OCT4 alone has been demonstrated to reprogram mouse fibroblasts into iPSCs. However, it remains unclear whether any other single factor can induce iPSCs formation.

Generation and characterization of giant panda induced pluripotent stem cells.

The giant panda () stands as a flagship and umbrella species, symbolizing global biodiversity. While traditional assisted reproductive technology faces constraints in safeguarding the genetic diversity of giant pandas, induced pluripotent stem cells (iPSCs) known for their capacity to differentiate into diverse cells types, including germ cells, present a transformative potential for conservation of endangered animals. In this study, primary fibroblast cells were isolated from the giant panda, and giant panda iPSCs (GPiPSCs) were generated using a non-integrating episomal vector reprogramming method.

Diagnostic performance of noninvasive imaging using computed tomography, magnetic resonance imaging, and positron emission tomography for the detection of ovarian cancer: a meta-analysis.

Objective: The aim of this meta-analysis was to compare the diagnostic value of noninvasive imaging methods computed tomography (CT), magnetic resonance imaging (MRI), and positron emission tomography (PET) in the detection of ovarian cancer (OC).

Methods: PubMed, Embase, and Ovid were comprehensively searched from the date of inception to 31st, March, 2022. Pooled sensitivity, specificity, positive likelihood ratio (+ LR), negative likelihood ratio (- LR), diagnostic odds ratio (DOR), and area under the curve (AUC) of summary receiver operating characteristic (SROC) with their respective 95% confidence intervals (CIs) were calculated.

Efficacy and safety of CD22-specific and CD19/CD22-bispecific CAR-T cell therapy in patients with hematologic malignancies: A systematic review and meta-analysis.

Background: CD22 single and CD19/CD22 bispecific targeted chimeric antigen receptor T (CAR-T) cell therapy are promising immunotherapy modalities for the treatment of hematologic malignancies. The aim of this study was to assess the efficacy and safety of CD22 and CD19/CD22 targeted CAR-T cell therapy by summarizing the existing evidence.

Methods: Electronic databases including PubMed, Embase, and Scopus were comprehensively searched from inception up to November 30, 2022.

Static Magnetic Fields Regulate T-Type Calcium Ion Channels and Mediate Mesenchymal Stem Cells Proliferation.

The static magnetic fields (SMFs) impact on biological systems, induce a variety of biological responses, and have been applied to the clinical treatment of diseases. However, the underlying mechanisms remain largely unclear. In this report, by using human mesenchymal stem cells (MSCs) as a model, we investigated the biological effect of SMFs at a molecular and cellular level.

CREB1 contributes colorectal cancer cell plasticity by regulating lncRNA CCAT1 and NF-κB pathways.

The CREB1 gene encodes an exceptionally pleiotropic transcription factor that frequently dysregulated in human cancers. CREB1 can regulate tumor cell status of proliferation and/or migration; however, the molecular basis for this switch involvement in cell plasticity has not fully been understood yet. Here, we first show that knocking out CREB1 triggers a remarkable effect of epithelial-mesenchymal transition (EMT) and leads to the occurrence of inhibited proliferation and enhanced motility in HCT116 colorectal cancer cells.

Cycle Flux Ranking of Network Analysis in Quantum Thermal Devices.

Manipulating quantum thermal transport relies on uncovering the principle working cycles of quantum devices. Here we introduce the cycle flux ranking of network analysis to nonequilibrium thermal devices characterized as a quantum-transition network. To excavate the principal mechanism out of complex transport behaviors, we decompose the network into cycle trajectories, collect the cycle fluxes by algebraic graph theory, and select top-ranked cycle fluxes, i.

miR-372 and miR-373 enhance the stemness of colorectal cancer cells by repressing differentiation signaling pathways.

miR-372/373, a cluster of stem cell-specific microRNAs transactivated by the Wnt pathway, has been reported to be dysregulated in various cancers, particularly colorectal cancer (CRC); however, the unique role of these microRNAs in cancer remains to be discovered. In the present study, we characterized the upregulation in expression of miR-372/373 in CRC tissues from The Cancer Genome Atlas data, and then showed that overexpression of miR-372/373 enhanced the stemness of CRC cells by enriching the CD26/CD24-positive cell population and promoting self-renewal, chemotherapy resistance and the invasive potential of CRC cells. To clarify the mechanism underlying microRNA-induced stemness, we profiled 45 cell signaling pathways in CRC cells overexpressing miR-372/373 and found that stemness-related pathways, such as Nanog and Hedgehog, were upregulated.

Wnt/β-catenin pathway transactivates microRNA-150 that promotes EMT of colorectal cancer cells by suppressing CREB signaling.

A hallmark of aberrant activation of the Wnt/β-catenin signaling pathway has been observed in most colorectal cancers (CRC), but little is known about the role of non-coding RNAs regulated by this pathway. Here, we found that miR-150 was the most significantly upregulated microRNA responsive to elevated of Wnt/β-catenin signaling activity in both HCT116 and HEK293T cells. Mechanistically, the β-catenin/LEF1 complex binds to the conserved TCF/LEF1-binding element in the miR-150 promoter and thereby transactivates its expression.

Triggering Fbw7-mediated proteasomal degradation of c-Myc by oridonin induces cell growth inhibition and apoptosis.

The transcription factor c-Myc is important in cell fate decisions and is frequently overexpressed in cancer cells, making it an attractive therapeutic target. Natural compounds are among the current strategies aimed at targeting c-Myc, but their modes of action still need to be characterized. To explore the mechanisms underlying the anticancer activity of a natural diterpenoid, oridonin, we conducted miRNA expression profiling and statistical analyses that strongly suggested that c-Myc was a potential molecular target of oridonin.