Breast cancer (BC) is a global health concern, and development of diagnostic tools and targeted treatments for BC remains challenging. Therapeutic approaches for BC often involve a combination of surgery, radiation therapy, chemotherapy, targeted therapy, and hormone therapy. In recent years, there has been a growing interest in the role of noncoding RNAs (ncRNAs), including long ncRNAs (lncRNAs) and microRNAs (miRNAs), in BC and their therapeutic implications. Various biological processes such as cell proliferation, migration, and apoptosis rely on the activities of these ncRNAs, and their dysregulation has been implicated in BC progression. The regulatory function of the competitive endogenous RNA (ceRNA) network, which comprises lncRNAs, miRNAs, and mRNAs, has been the subject of extensive pathophysiological research. Most lncRNAs serve as molecular sponges for miRNAs and sequester their activities, thereby regulating the expression of target mRNAs and contributing to the promotion or inhibition of BC progression. This review summarizes recent findings on the role of ceRNA networks in BC progression, metastasis, and therapeutic resistance, and highlights the association of ceRNA networks with transcription factors and signaling pathways. Understanding the ceRNA network can lead to the discovery of biomarkers and targeted treatment methods to prevent the spread and metastasis of BC. 

Regulatory and therapeutic implications of competing endogenous RNA network in breast cancer progression and metastasis: A review

As an important nutrient in the human body, cholesterol can not only provide structural components for the body's cells, but also can be transformed into a variety of active substances to regulate cell signaling pathways. As an important cholesterol synthase, DHCR24 participates in important regulatory processes in the body. The application of DHCR24 in tumor clinical diagnosis and treatment also attracts much attention. This article reviews the structure and regulatory characteristics of DHCR24, and the research of DHCR24 on tumor progression. We summarize the possible mechanisms of DHCR24 promoting tumor progression through reactive oxygen species (ROS), p53, Ras and PI3K-AKT pathways. Through our review, we hope to provide more research ideas and reference value for the application of DHCR24 in tumor prevention and treatment.

DHCR24 in Tumor Diagnosis and Treatment: A Comprehensive Review

Primordial germ cells (PGCs), as the precursors of gametes found in early embryos, provide a new direction for solving the problem of reproductive disorders. In vitro, conversion of adult stem cells (ASCs) into primordial germ cell-like cells (PGCLCs) is feasible. The means of increasing PGCLCs number in vitro has been a focus of recent stem cell research. In this study, we found that luteinizing hormone (LH) could promote porcine PGCLCs (pPGCLCs) proliferation. To investigate the proliferation regulatory network, whole transcriptome sequencing technology was employed. Results showed that the TGF-β signaling pathway played a key role. In addition, we found that TGFβR1 and SMAD4, TGF-β signaling pathway-related genes, were significantly upregulated after LH treatment. Subsequently, we predicted their target microRNAs (miRNAs) and long non-coding RNAs (lncRNAs): ssc-miR-128, ssc-miR-146b, ssc-miR-361-3p, MSTRG.11473, MSTRG.11475, MSTRG.11553, and MSTRG.11554, and constructed the competitive endogenous RNAs (ceRNA) network. Finally, to further verify the ceRNA network, the miRNA-inhibitors were transfected into cells. RT-qPCR results indicated a significant increase in the expression of MSTRG.11473, MSTRG.11475, MSTRG.11553, MSTRG.11554, TGFβR1, and SMAD4 compared to the negative control (NC) group. In conclusion, these results highlight that LH could regulate the pPGCLCs proliferation by modulating the expression of TGF-β signaling pathway-related ncRNAs. 

LH promotes the proliferation of porcine primordial germ cell-like cells (pPGCLCs) by regulating the ceRNA network related to the TGF-β signaling pathway

Upregulation of DHCR24 in cervical cancer promotes cervical cancer development and correlates with immune infiltration and tumor stemness

We present an innovative strategy for integrating whole-genome-wide multi-omics data, which facilitates adaptive amalgamation by leveraging hidden layer features derived from high-dimensional omics data through a multi-task encoder. Empirical evaluations on eight benchmark cancer datasets substantiated that our proposed framework outstripped the comparative algorithms in cancer subtyping, delivering superior subtyping outcomes. Building upon these subtyping results, we establish a robust pipeline for identifying whole-genome-wide biomarkers, unearthing 195 significant biomarkers. Furthermore, we conduct an exhaustive analysis to assess the importance of each omic and non-coding region features at the whole-genome-wide level during cancer subtyping. Our investigation shows that both omics and non-coding region features substantially impact cancer development and survival prognosis. This study emphasizes the potential and practical implications of integrating genome-wide data in cancer research, demonstrating the potency of comprehensive genomic characterization. Additionally, our findings offer insightful perspectives for multi-omics analysis employing deep learning methodologies. 

Subtype-WGME enables whole-genome-wide multi-omics cancer subtyping.

Krüppel-like zinc-finger transcription factor 5 (KLF5) is a vital regulator of breast cancer (BC) onset and progression. The mechanism by which KLF5 regulates BC is still not clearly known. In this study, bioinformatics analysis shows that BC-affected individuals with elevated KLF5 expression levels have poor clinical outcomes. We further verify that miR-145-5p regulated KLF5 expression to promote cell apoptosis and inhibit cell proliferation in BC via dual-luciferase reporter assay, western blot analysis, qRT-PCR, CCK-8 assay and cell apoptosis assay. In addition, based on bioinformatics analysis, the binding of ENST00000422059 with miR-145-5p is confirmed by dual-luciferase reporter assay. Subsequently, FISH, western blot analysis, qRT-PCR, CCK-8 and cell apoptosis assays verified that ENST00000422059 increases KLF5 protein expression by sponging miRNA to promote cell proliferation and inhibit cell apoptosis. Finally, ENST00000422059 is found to accelerate tumor progression by regulating the miR-145-5p/KLF5 axis in vivo. In conclusion, this study suggests that ENST00000422059 upregulates KLF5 by sponging miR-145-5p to promote BC progression.

lncRNA ENST00000422059 promotes cell proliferation and inhibits cell apoptosis in breast cancer by regulating the miR-145-5p/KLF5 axis.

Long noncoding RNAs (lncRNAs) are critically involved in the occurrence and development of breast cancer (BC). In this study, we performed RNA sequencing, and the results revealed an increase in the expression level of novel lncRNA ENST00000370438 in tissues of patients with BC. Quantitative reverse transcription polymerase chain reaction (qRT‐PCR) results showed an increase in lncRNA ENST00000370438 expression level in 23 pairs of BC tissues. Next, we determined the effect of ENST00000370438 on BC cell proliferation, and the results showed that ENST00000370438 promotes cell proliferation in BC. The proteomic analysis showed a decrease in DHCR24 expression level in BC cells transfected with ENST00000370438 small interfering RNA. Western blot and qRT‐PCR assay results showed that ENST00000370438 regulated DHCR24 expression. Furthermore, the rescue experiment showed that the interference with ENST00000370438 expression could restore the effect of DHCR24 overexpression on BC cell proliferation, demonstrating that ENST00000370438 could promote cell proliferation by upregulating DHCR24. Finally, we showed that lncRNA ENST000000370438 could promote tumor growth by overexpressing DHCR24 in nude mice. Our results demonstrated that lncRNA ENST00000370438 promotes BC cell proliferation by upregulating DHCR24 expression.

LncRNA ENST00000370438 promotes cell proliferation by upregulating DHCR24 in breast cancer

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lncRNA ENST00000422059 promotes cell proliferation and inhibits cell apoptosis in breast cancer by regulating the miR-145-5p/KLF5 axis.

LncRNA ENST00000370438 promotes cell proliferation by upregulating DHCR24 in breast cancer