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. 2021 Oct 15;18(sup1):369-381.
doi: 10.1080/15476286.2021.1950464. Epub 2021 Aug 10.

LncRNA CASC21 induces HGH1 to mediate colorectal cancer cell proliferation, migration, EMT and stemness

Chenxin Zhang  1   2 , Jifu E  2 , Enda Yu  2
Affiliations

LncRNA CASC21 induces HGH1 to mediate colorectal cancer cell proliferation, migration, EMT and stemness

Chenxin Zhang et al. RNA Biol. .

Abstract

Colorectal cancer (CRC) is one of the leading causes of cancer-related deaths worldwide. Long non-coding RNAs (lncRNAs) have been increasingly reported to serve vital parts in malignancies including CRC. Although cancer susceptibility 21 (CASC21) has been uncovered to play a part in CRC, its mechanism still needs further explanation. Thus, our study aimed to further explore the influence and mechanism of CASC21 in CRC progression. Quantitative real-time RT-PCR and western blot were performed to detect gene expression; a series of functional assays were performed to investigate the effect of CASC21 on CRC cells; in vivo tumour growth was evaluated via the nude mice xenograft model. The results revealed that CASC21 facilitated CRC cell proliferation, migration, epithelial-mesenchymal transition (EMT) and stemness. In addition, CASC21 was co-expressed with and bound to transcription factor POU5F1B (POU class 5 homeobox 1B). CASC21 recruited POU5F1B to HGH1 promoter to activate the transcription of HGH1 homolog. Also, CASC21 served as a competitive endogenous RNA (ceRNA) to up-regulate HGH1 via endogenously sponging miR-485-5p. Moreover, HGH1 overexpression counteracted the suppression of CASC21 deficiency on CRC tumour growth. In summary, our study indicated that CASC21 enhanced the expression of HGH1 to promote the malignancy of CRC by recruiting POU5F1B and sponging miR-485-5p, suggesting a key role of CASC21 in CRC progression.

Keywords: CASC21; Colorectal cancer; HGH1; POU5F1B; miR-485-5p.

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Conflict of interest statement

No potential conflict of interest was reported by the author(s).

Figures

None
Graphical abstract
Figure 1.
Figure 1.
CASC21 expression was up-regulated in CRC tissues and cells
Figure 2.
Figure 2.
CASC21 inhibition suppressed CRC cell proliferation, migration, EMT and stemness
Figure 3.
Figure 3.
CASC21 bound to POU5F1B to synergistically up-regulate HGH1
Figure 4.
Figure 4.
CASC21 cooperated with POU5F1B to activate the transcription of HGH1
Figure 5.
Figure 5.
CASC21 sponged miR-485-5p to elevate HGH1
Figure 6.
Figure 6.
HGH1 mediated the function of CASC21 in regulating CRC cell proliferation, migration, EMT and stemness
Figure 7.
Figure 7.
CASC21 depended on HGH1 to promote CRC tumour growth in vivo.
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References

    1. Bray F, Ferlay J, Soerjomataram I, et al. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin. 2018;68(6):394–424. - PubMed
    1. Siegel RL, Miller KD, Jemal A.. Cancer Statistics, 2017. CA Cancer J Clin. 2017;67(1):7–30. - PubMed
    1. Watson AJ, Collins PD. Colon cancer: a civilization disorder. Dig Dis. 2011;29(2):222–228. - PubMed
    1. Liang ZX, Liu H-S, Wang F-W, et al. LncRNA RPPH1 promotes colorectal cancer metastasis by interacting with TUBB3 and by promoting exosomes-mediated macrophage M2 polarization. Cell Death Dis. 2019;10(11):829. - PMC - PubMed
    1. Ni W, Yao S, Zhou Y, et al. Long noncoding RNA GAS5 inhibits progression of colorectal cancer by interacting with and triggering YAP phosphorylation and degradation and is negatively regulated by the m(6)A reader YTHDF3. Mol Cancer. 2019;18(1):143. - PMC - PubMed

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