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Comment
. 2021 Feb 22;6(1):84.
doi: 10.1038/s41392-021-00497-4.

Therapeutic potential of C1632 by inhibition of SARS-CoV-2 replication and viral-induced inflammation through upregulating let-7

Chen Xie #  1 , Yanlian Chen #  1 , Dongling Luo  2 , Zhen Zhuang  3 , Heping Jin  1 , Haoxian Zhou  1 , Xiaocui Li  1 , Haijun Lin  4 , Xiaohui Zheng  5 , Jing Zhang  6 , Peihui Wang  6 , Jincun Zhao  3 , Yong Zhao  7 , Hui Huang  8
Affiliations
Comment

Therapeutic potential of C1632 by inhibition of SARS-CoV-2 replication and viral-induced inflammation through upregulating let-7

Chen Xie et al. Signal Transduct Target Ther. .
No abstract available

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Validation of C1632 as a potential anti-SARS-CoV-2 drug that suppresses both virus replication and viral-induced inflammation by upregulating let-7. Let-7 inhibits exogenous expression of S protein (a) and M protein (b) in HEK293T cells. GFP was cloned into vector to ensure the equal transfection/expression efficiency. Scramble sequence was used as a control. c The expression level of IL-1β, IL-6, IL-8, CCL2, GM-CSF, TNF-α, and VEGFα were downregulated by overexpressed let-7a and let-7c in THP1 cells. d let-7-5p and let-7-3p sponges increased the expression level of multiple inflammatory factors in THP1 cells. let-7 stimulator C1632 inhibited exogenous expression of S (e) and M (f) protein in HEK293T cells in a concentration dependent manner. g–i The expression of IL-1β, IL-6, IL-8, CCL2, GM-CSF, and VEGFα were downregulated by C1632 in THP1 derived macrophages (g) and PBMCs (h). i The expression of IL-1β, IL-6, IL-8, CCL2, GM-CSF, TNF-α, and VEGFα were downregulated by C1632 in Huh-7 cells. The RNA level of N (j) and ORF1 (k) were suppressed by C1632 in a dosage dependent manner in SARS-CoV-2 infected Huh-7 cells. l C1632 treatment decreased S protein level in SARS-CoV-2 infected Huh-7 cells (western blot). The expression level of IL-6 (m), IL-8 (n), TNF-α (o) and CCL2 (p) were downregulated by C1632 in SARS-CoV-2 infected Huh-7 cells
See this image and copyright information in PMC

Comment on

References

    1. Merad M, et al. Pathological inflammation in patients with COVID-19: a key role for monocytes and macrophages. Nat. Rev. Immunol. 2020;20:355–362. doi: 10.1038/s41577-020-0331-4. - DOI - PMC - PubMed
    1. Pedersen IM, et al. Interferon modulation of cellular microRNAs as an antiviral mechanism. Nature. 2007;449:919–922. doi: 10.1038/nature06205. - DOI - PMC - PubMed
    1. Iliopoulos D, et al. Struhl, an epigenetic switch involving NF-κB, Lin28, Let-7 microRNA, and IL6 links inflammation to cell transformation. Cell. 2009;139:693–706. doi: 10.1016/j.cell.2009.10.014. - DOI - PMC - PubMed
    1. Roos M, et al. A small-molecule inhibitor of Lin28. ACS Chem. Biol. 2016;11:2773–2781. doi: 10.1021/acschembio.6b00232. - DOI - PubMed
    1. Chen Y, et al. LIN28/let-7/PD-L1 pathway as a target for cancer immunotherapy. Cancer Immunol. Res. 2019;7:487–497. doi: 10.1158/2326-6066.CIR-18-0331. - DOI - PubMed