Pou2F3 silencing enhanced the proliferation of mammary epithelial cells in dairy goat via PI3K/AKT/mTOR signaling pathway

Liu, Shujuan; Cao, Heran; Guo, Dan; Yin, Hao; Zhu, Junru; Duan, Qiangde; Seleh‐Zo, Emeline; Li, Guang; An, Xiaopeng; Cao, Binyun

doi:10.1080/10495398.2020.1798974

Cited by 2 publications

(3 citation statements)

References 30 publications

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“…Furthermore, we next conducted SCENIC analysis to identify the decisive regulators of the epithelial subsets between HSIL and CA (Figure 2J). Strikingly, BRCA1, 25 which play a crucial role in DNA replication, DNA repair and genomic stability maintenance, 26 predominantly regulates the HPV‐related HSIL cluster, whereas TP63, ELF3 and POU2F3 modulate the abnormal proliferation and differentiation of epithelial cells in the HPV‐related CA cluster 27,28 . Overall, we creatively discovered 12 critical node genes and 5 regulons during the progression from the HPV‐infected normal cervix to HSIL to CA.…”

Section: Resultsmentioning

confidence: 93%

“…Strikingly, BRCA1, 25 which play a crucial role in DNA replication, DNA repair and genomic stability maintenance, 26 predominantly regulates the HPV‐related HSIL cluster, whereas TP63, ELF3 and POU2F3 modulate the abnormal proliferation and differentiation of epithelial cells in the HPV‐related CA cluster. 27 , 28 Overall, we creatively discovered 12 critical node genes and 5 regulons during the progression from the HPV‐infected normal cervix to HSIL to CA. These findings could facilitate accurate molecular subtyping and provide novel insights for the precise intervention of cervical lesions and tumours in clinical practice.…”

Section: Resultsmentioning

confidence: 99%

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Spatiotemporally deciphering the mysterious mechanism of persistent HPV‐induced malignant transition and immune remodelling from HPV‐infected normal cervix, precancer to cervical cancer: Integrating single‐cell RNA‐sequencing and spatial transcriptome

Guo

Tang

et al. 2023

Clinical & Translational Med

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Background The mechanism underlying cervical carcinogenesis that is mediated by persistent human papillomavirus (HPV) infection remains elusive. Aims Here, for the first time, we deciphered both the temporal transition and spatial distribution of cellular subsets during disease progression from normal cervix tissues to precursor lesions to cervical cancer. Materials & Methods We generated scRNA‐seq profiles and spatial transcriptomics data from nine patient samples, including two HPV‐negative normal, two HPV‐positive normal, two HPV‐positive HSIL and three HPV‐positive cancer samples. Results We not only identified three ‘HPV‐related epithelial clusters’ that are unique to normal, high‐grade squamous intraepithelial lesions (HSIL) and cervical cancer tissues but also discovered node genes that potentially regulate disease progression. Moreover, we observed the gradual transition of multiple immune cells that exhibited positive immune responses, followed by dysregulation and exhaustion, and ultimately established an immune‐suppressive microenvironment during the malignant program. In addition, analysis of cellular interactions further verified that a ‘homeostasis‐balance‐malignancy’ change occurred within the cervical microenvironment during disease progression. Discussion We for the first time presented a spatiotemporal atlas that systematically described the cellular heterogeneity and spatial map along the four developmental steps of HPV‐related cervical oncogenesis, including normal, HPV‐positive normal, HSIL and cancer. We identified three unique HPV‐related clusters, discovered critical node genes that determined the cell fate and uncovered the immune remodeling during disease escalation. Conclusion Together, these findings provided novel possibilities for accurate diagnosis, precise treatment and prognosis evaluation of patients with precancer and cervical cancer.

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Section: Resultsmentioning

confidence: 93%

Section: Resultsmentioning

confidence: 99%

Spatiotemporally deciphering the mysterious mechanism of persistent HPV‐induced malignant transition and immune remodelling from HPV‐infected normal cervix, precancer to cervical cancer: Integrating single‐cell RNA‐sequencing and spatial transcriptome

Guo

Tang

et al. 2023

Clinical & Translational Med

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“…Nevertheless, the role of HSP47 in NSCLC remains to be explored. Furthermore, protein kinase B (AKT) signaling is implicated in a number of fundamental cellular processes, including proliferation [17] and survival [18]. Moreover, AKT also plays a regulatory role in angiogenesis and metabolism [19], in addition to modulating various cellular survival pathways, primarily as an inhibitor of apoptosis [20].…”

Section: Introductionmentioning

confidence: 99%

Heat shock protein 47 promotes cell migration and invasion through AKT signal in non-small cell lung cancer

Xiong

et al. 2021

Anti-Cancer Drugs

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Lung cancer is one of the most lethal malignancies, with the highest number of cases and deaths. Non-small cell lung cancer (NSCLC) is the most ordinary type of pathology in lung cancer. Meanwhile, various researchers have reported that heat shock protein 47 (HSP47) plays a vital regulatory role in cancer. However, the role of HSP47 in NSCLC is not clear. Consequently, the current study set out to investigate the role of HSP47 in the pathogenesis of NSCLC. First, we evaluated the expression patterns of HSP47 in NSCLC cell lines related to human normal lung epithelial cells, and HSP47 was found to be highly expressed in NSCLC cell lines. In addition, inhibiting the expression of HSP47 brought about marked repression in cell proliferation, migration and invasion in PC-9 cells. On the contrary, cell proliferation, migration and invasion were all elevated after over-expression of HSP47. Mechanistical experimentation further illustrated that protein kinase B (AKT) signal was repressed after inhibition of HSP47, and the influence of sh-HSP47 on cell proliferation, migration and invasion was countered by epidermal growth factor. Lastly, in-vivo animal models demonstrated that inhibition of HSP47 repressed cell tumorigenesis and AKT signal. Collectively, our findings illustrated that HSP47 was highly expressed in NSCLC cell lines, whereas inhibition of HSP47 repressed cell migration and invasion by diminishing the AKT signal. Inhibition of HSP47 also exhibited strong therapeutic effects on NSCLC in vivo

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Pou2F3 silencing enhanced the proliferation of mammary epithelial cells in dairy goat via PI3K/AKT/mTOR signaling pathway

Cited by 2 publications

References 30 publications

Spatiotemporally deciphering the mysterious mechanism of persistent HPV‐induced malignant transition and immune remodelling from HPV‐infected normal cervix, precancer to cervical cancer: Integrating single‐cell RNA‐sequencing and spatial transcriptome

Spatiotemporally deciphering the mysterious mechanism of persistent HPV‐induced malignant transition and immune remodelling from HPV‐infected normal cervix, precancer to cervical cancer: Integrating single‐cell RNA‐sequencing and spatial transcriptome

Heat shock protein 47 promotes cell migration and invasion through AKT signal in non-small cell lung cancer

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