Biodiversity Informatics
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Interleukin-6 regulates expression of estrogen receptors in human colorectal cancer and acute T-cell leukemia cells
Interleukin-6 (IL-6) is a pleiotropic cytokine involved in inflammation, immune regulation, and tumor progression. Estrogen receptors (ERs), particularly ERα and ER, play distinct roles in modulating immune responses and cancer development, yet their regulation by IL-6 in different cancer types remains incompletely understood. In this study, we investigated the effects of IL-6 on expression of ERα and ERβ in human colorectal cancer cells (HCT116) and acute T-cell leukemia cells (Jurkat). The cells were treated with recombinant human IL-6 (at a dosage of 100 ng/ml) for up to 24 hours, and changes in ER expression were assessed using Western blot analysis. We found that IL-6 treatment did not significantly alter ERα or ERβ levels in HCT116 cells, though a non-significant upward trend in ERβ expression was observed. In contrast, Jurkat cells exhibited a statistically significant increase in ERβ expression at 8 and 24 hours after IL-6 stimulation, while ERα expression remained unchanged. These findings suggest a cell-type-specific regulatory role of IL-6 in modulating estrogen receptor expression. The selective upregulation of ERβ in Jurkat cells implies a potential IL-6-ERβ signaling axis in T-cell leukemia, which may contribute to inflammation-driven leukemogenesis and warrants further mechanistic investigation
Interactions between Pro-inflammatory Cytokines and Estrogen Receptors in Endometrial Cancer
Endometrial cancer (EC) is a hormone-driven malignancy in which estrogen receptor (ER) signaling plays a central role. Meanwhile, chronic inflammation, particularly mediated by pro-inflammatory cytokines such as interleukin-6 (IL-6) and interleukin-17 (IL-17), has emerged as a key contributor to endometrial cancer progression. This review examines the interplay between IL-6, IL-17, and estrogen receptors (ERα and ERβ) in endometrial cancer cells, highlighting how these cytokines regulate ER expression and function through multiple signaling pathways, including the Janus kinase/signal transducer and activator of transcription (JAK/STAT), nuclear factor-κB (NF-κB), and mitogen-activated protein kinase (MAPK) pathways. IL-6 and IL-17 have been shown to upregulate ERα and suppress ERβ, thereby enhancing estrogen-mediated tumor proliferation and potentially contributing to hormonal therapy resistance. Moreover, evidence suggests a bidirectional feedback loop in which estrogen signaling further amplifies cytokine production, creating a self-sustaining inflammatory environment that promotes tumor progression. Understanding this cytokine–ER crosstalk provides novel insights into endometrial cancer pathogenesis and reveals potential therapeutic targets. Strategies that combine endocrine therapy with anti-inflammatory agents or cytokine pathway inhibitors may help overcome resistance and improve clinical outcomes in selected patients. Further mechanistic studies and clinical trials are needed to validate the prognostic and therapeutic relevance of IL-6 and IL-17 in hormone-responsive endometrial cancer
Competency-based Education Through Micro-credentials Offerings – A Pilot Study
This pilot study examined the implementation of Competency-Based Education (CBE) through micro-credentials at the Singapore Institute of Technology (SIT), focusing on the perspectives of learners, instructors, and employers. Despite a growing global interest in CBE, empirical research on its effectiveness remains limited. SIT’s Competency-Based Stackable Micro-credential (CSM) program offers modular, industry-relevant learning for working adults, with micro-credentials functioning as standalone qualifications or stackable units toward a full degree. Findings from learner surveys indicated that the content was highly relevant to real-world jobs, and the learning could be applied to work. Instructors recognized the relevance of CBE to industry needs, despite the increased demands associated with content development, delivery, and learner support. Employers observed improvements in employee competencies and workplace engagement. The findings underscore the potential of CBE micro-credentials to offer flexible, industry-focused education pathways when supported by robust frameworks and comprehensive learner support services.
Standardized protocol for collecting community-level bee data
A key component of assessing bee biodiversity patterns and supporting bee conservation is documenting bee communities. When integrated with additional ecological data, community-level data help reveal the relative impact of local- and landscape-scale factors on bee taxa. As such, these data can inform management decisions to support bee diversity and mitigate environmental drivers of decline. However, methods for sampling bee communities vary greatly across projects, making it difficult to compare existing datasets or design new, interoperable studies. Here, we provide a standardized protocol for collecting community-level bee biodiversity data and offer guidance on inventorying, surveying, and monitoring of bee communities. We also present case studies to illustrate how different components of the protocol could be implemented. Although we discuss the benefits of collecting physical specimens, we emphasize the importance of responsible collecting and highlight key strategies to minimize environmental impact while maximizing the value of the work in new projects. This protocol is part of a series developed in association with the U.S. National Native Bee Monitoring Network to standardize bee monitoring practices.
First report of gynandromorphy in Hoplitis: A bilateral specimen of Hoplitis (Alcidamea) producta (Hymenoptera: Megachilidae)
A bilateral gynandromorph of Hoplitis (Alcidamea) producta (Cresson) is described and illustrated for the first time. The specimen is notable for its nearly complete bilateral asymmetry and represents the first recorded case of gynandromorphism in Hoplitis. A summary of literature records on gynandromorphic bees is provided.