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In MCF7 LTED cells stably expressing both PIK3R1-Flag and doxycycline-inducible PIK3R1-HA, knockdown of PRR11 resulted in an increase of the p85 homodimers (Fig. 5g and Supplementary Fig. 6c). PRR11 silencing also reduced insulin-mediated association of p110α with IRS1 and insulin/IGF-stimulated p-AKT in MCF7 LTED and HCC1428 LTED cells (Fig. 5h, j and Supplementary Fig. 6d). Conversely, PRR11 overexpression enhanced the p110α-IRS1 association and p-AKT in MDA-MB-175VII cells (Fig. 5i, j). If you prefer the thrill of real-time action, the live casino section at RICH11 COM is where you need to be.

PLA was performed with Duolink In Situ Red Starter Kit Mouse/Rabbit (Sigma) according to the manufacturer’s protocol and then imaged with a DMi8 inverted microscope (Leica). The number of PLA foci was quantified by Duolink Image Tool software; 5 images per sample were analyzed. RNA was extracted from cells using Maxwell RSC simplyRNA Cells Kit (Promega) according to the manufacturer’s protocol.

Number of cells were counted with Z2 coulter counter analyzer (Beckman coulter). Four-μm tissue sections were mounted on charged slides and hybridized overnight with a PRR11 FISH probe (EMPIRE GENOMICS) and a centromere 17 control probe (EMPIRE GENOMICS); FISH was performed as described previously14. Twenty to sixty tumor cell nuclei from random areas were individually evaluated with the 100× oil immersion objective by counting green PRR11 and orange centromere 17 (CEN17) signals. The latest version, UPDF 2.0, introduces AI-powered features such as PDF summarization, translation, and interactive Q&A, enhancing the user experience. LTD., aiming to provide a comprehensive, user-friendly PDF solution accessible to everyone. Unlike many premium PDF editors, PDFgear offers a full suite of features—including text editing, OCR, annotation, conversion, and AI assistance—completely free of charge.

To explore this, we first utilized MCF10A cells that require EGF and insulin to propagate. PIK3CA knockdown significantly inhibited the proliferation of MCF10A cells grown in media containing EGF/insulin or insulin alone (Supplementary Fig. 8a, b). PIK3CA knockdown abolished growth promoted by PRR11 overexpression, suggesting that PRR11-mediated cell growth requires PIK3CA.

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• Then the cells’ cell cycle was analyzed on a BD FACS Calibur (Becton, Dickinson and Company, United States).
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• To our knowledge, this is the first study demonstrating the common regulation role of PRR11 on PTTG1 in different human cancer cells.
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Notably, PRR11 may play an oncogenic role in pan-cancer progression by regulating the expression of PTTG1 to involve in the cell cycle. In mechanism, PRR11 could combine with E2F1 to the E2F1 binding site of the PTTG1 promoter region, which consequently could stimulate the expression of PTTG1. To our knowledge, this is the first study demonstrating the common regulation role of PRR11 on PTTG1 in different human cancer cells.

Thus, PRR11 silencing in pan-cancers could suppress the expression level of PTTG1. Many cyclins and cyclin-related genes, including CCNA1, RRM1, PCNA (Ji et al., 2013), CDK6, CCNE, CCNA2, and CCNB2, were inhibited when interfering with PRR11 (Zhang et al., 2018). In addition, the low-expressed PRR11 could also suppress the expression level of apoptotic proteins, such as P62 (Zhang et al., 2018). Proline rich 11 (PRR11), initially renowned for its relevance with cell-cycle progression, is a proline-rich protein coding gene in chromosome 17q22-23. In particular, PRR11 also serves as a promising prognostic indicator in a limited number of human cancers, gradually manifesting its potential application for targeted therapies.

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