Targeting ninjurin 2 by miR-764 regulates hydrogen peroxide (H2O2)-induced neuronal cell death

Jing, Ding; Yinzhu, Li; Jinjing, Pang; Liang, Li‐Jung; Zhang, Guozhuan

doi:10.1016/j.bbrc.2018.09.184

Cited by 19 publications

(25 citation statements)

References 27 publications

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“…Ninj1 has been reported to play an important role in the maintenance of bone and muscle homeostasis, as well as in the regulation of leukocyte trafficking into neuroinflammatory lesions 29‐32 . Ninj2 has been reported to protect neuronal cells from hydrogen peroxide and regulates endothelial inflammation and activation 33,34 . Moreover, both proteins have been associated with colon cancer.…”

Section: Introductionmentioning

confidence: 99%

Ninjurin1 deficiency aggravates colitis development by promoting M1 macrophage polarization and inducing microbial imbalance

et al. 2020

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Disruption of colonic homeostasis caused by aberrant M1/M2 macrophage polarization and dysbiosis contributes to inflammatory bowel disease (IBD) pathogenesis. However, the molecular factors mediating colonic homeostasis are not well characterized. Here, we found that Ninjurin1 (Ninj1) limits colon inflammation by regulating macrophage polarization and microbiota composition under homeostatic conditions and during colitis development. Ninj1 deletion in mice induced hypersusceptibility to colitis, with increased prevalence of colitogenic Prevotellaceae strains and decreased immunoregulatory Lachnospiraceae strains. Upon co‐housing (CoH) with WT mice, Ninj1−/− mice showed increased Lachnospiraceae and decreased Prevotellaceae abundance, with subsequent improvement of colitis. Under homeostatic conditions, M1 macrophage frequency was higher in the Ninj1−/− mouse colons than wild‐type (WT) mouse colons, which may contribute to increased basal colonic inflammation and microbial imbalance. Following colitis induction, Ninj1 expression was increased in macrophages; meanwhile Ninj1−/− mice showed severe colitis development and impaired recovery, associated with decreased M2 macrophages and escalated microbial imbalance. In vitro, Ninj1 knockdown in mouse and human macrophages activated M1 polarization and restricted M2 polarization. Finally, the transfer of WT macrophages ameliorated severe colitis in Ninj1−/− mice. These findings suggest that Ninj1 mediates colonic homeostasis by modulating M1/M2 macrophage balance and preventing extensive dysbiosis, with implications for IBD prevention and therapy.

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Section: Introductionmentioning

confidence: 99%

Ninjurin1 deficiency aggravates colitis development by promoting M1 macrophage polarization and inducing microbial imbalance

et al. 2020

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“…Liu et al , have shown that NINJ2 expression is important for the survival of neuronal cells [16]. Very recently, Jing et al, demonstrated that ectopic NINJ2 overexpression protected neuronal cells from hydrogen peroxide (H 2 O 2 ) [17]. To our best knowledge, NINJ2’s expression and potential functions in CRC and other human cancers have not been studied thus far.…”

Section: Discussionmentioning

confidence: 99%

Ninjurin 2 overexpression promotes human colorectal cancer cell growth in vitro and in vivo

Zhou

Han

et al. 2019

Aging

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Ninjurin 2 (NINJ2) is a novel adhesion molecule. Its expression and potential function in human colorectal cancer (CRC) cells are studied. We show that NINJ2 is overexpressed in established (HT-29) and primary CRC cells and in human colon cancer tissues. Its expression level is low in colon epithelial cells and normal colon tissues. NINJ2 shRNA or knockout (by CRSIPR/Cas9) potently inhibited human CRC cell survival and proliferation, while significantly inducing cell apoptosis. Conversely, lentivirus-mediated NINJ2 overexpression promoted CRC cell proliferation. NINJ2 co-immunoprecipitated with multiple RTKs (EGFR, PDGFRα/β and FGFR) in CRC cells and human colon cancer tissues. In HT-29 cells, RTKs’ downstream signalings, Akt and Erk, were significantly inhibited by NINJ2 shRNA or knockout, but augmented following ectopic NINJ2 overexpression. In vivo, NINJ2-silenced or NINJ2-knockout CRC xenografts grew significantly slower than the control xenografts. Akt-Erk activation was largely inhibited in CRC xenografts with NINJ2 silencing or knockout. Taken together, NINJ2 overexpression promotes CRC cell growth in vitro and in vivo.

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“…The established A172 glioma cells were provided by Dr. Cao 19 . Brain cortical tissues were obtained from 15-week-old normal fetal brains (prepared from Dr. Zhang 20 ), dissociated, digested, and filtered as previously described 21,22 . The dissociated cells were centrifuged and resuspended in MEM medium with applied supplements 22 .…”

Section: Methodsmentioning

confidence: 99%

Circular RNA PRKCI promotes glioma cell progression by inhibiting microRNA-545

Zhang

Han

et al. 2019

Cell Death Dis

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We here tested expression and potential functions of circular RNA PRKCI (circPRKCI) in human glioma. Our results show that circPRKCI is upregulated in human glioma tissues and glioma cells, correlating with downregulation of its potential target, microRNA-545 (miR-545). In A172 and primary human glioma cells, shRNA-mediated silencing of circPRKCI inhibited cancer cell growth, survival, proliferation, and migration. Conversely, ectopic circPRKCI overexpression promoted A172 cell progression. miR-545 is the primary target of circPRKCI in glioma cells. Forced overexpression of miR-545 mimicked circPRKCI shRNA-induced actions, inhibiting glioma cell survival and proliferation. In contrast, miR-545 inhibition, by a lentiviral antagomiR-545 construct, reversed circPRKCI shRNA-induced anti-A172 cell activity. Importantly, neither circPRKCI shRNA nor circPRKCI overexpression was effective in miR-545-knockout (Cas9 method) A172 cells. Importantly, the subcutaneous and orthotopic A172 xenograft growth was significantly inhibited by circPRKCI silencing. Collectively, circPRKCI promotes human glioma cell progression possibly by inhibiting miR-545. Targeting circPRKCI-miR-545 cascade could efficiently inhibit human glioma cells.

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Targeting ninjurin 2 by miR-764 regulates hydrogen peroxide (H2O2)-induced neuronal cell death

Cited by 19 publications

References 27 publications

Ninjurin1 deficiency aggravates colitis development by promoting M1 macrophage polarization and inducing microbial imbalance

Ninjurin1 deficiency aggravates colitis development by promoting M1 macrophage polarization and inducing microbial imbalance

Ninjurin 2 overexpression promotes human colorectal cancer cell growth in vitro and in vivo

Circular RNA PRKCI promotes glioma cell progression by inhibiting microRNA-545

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