ANKRD49 inhibits etoposide-induced intrinsic apoptosis of GC-1 cells by modulating NF-κB signaling

Zhou, Xia; Wang, Wentao; Sun, Jia; Liu, Hongyan; Bai, Xin-Yan; Liu, Juanjuan; Yu, Bin; Guo, Rui; Wang, Hailong

doi:10.1007/s11010-019-03508-9

Cited by 6 publications

(7 citation statements)

References 39 publications

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“…Notably, the NF‐κB signaling pathway was enriched (Figure 6B), and the DEGs were involved in cell adhesion, cell death, extracellular matrix organization and EMT, as indicated by GO analysis (Figure 6C). It has been reported that ankyrin repeat proteins can regulate the NF‐κB pathway, 21 and that the ANKRD protein family can regulate NF‐κB signaling pathway, 15,22,23 and also that the NF‐κB signaling pathway is involved in regulating EVT functions 24 . Therefore, we further explored the effects of ANKRD37 on NF‐κB signaling using Western blotting to detect the IκBα and p65 phosphorylation levels.…”

Section: Resultsmentioning

confidence: 99%

“…For example, ANKRD26 can regulate kisspeptin‐GPR54 signaling to mediate neuronal movement by inhibiting cell migration 14 . ANKRD49 can inhibit the apoptosis of GC‐1 spermatogonia through the nuclear factor‐kappa B (NF‐κB) signaling pathway and participates in spermatogenesis 15 . ANKRD37 is a member of the ANKRD protein family that is degraded through the ubiquitin system mediated by Fem1b 16 , and is involved in regulating cell growth and HIF‐1a‐induced autophagy in colon cancer 17 .…”

Section: Introductionmentioning

confidence: 99%

“…14 ANKRD49 can inhibit the apoptosis of GC-1 spermatogonia through the nuclear factor-kappa B (NF-κB) signaling pathway and participates in spermatogenesis. 15 ANKRD37 is a member of the ANKRD protein family that is degraded through the ubiquitin system mediated by Fem1b 16 , and is involved in regulating cell growth and HIF-1a-induced autophagy in colon cancer. 17 A previous study revealed that ANKRD37 was significantly increased in testosterone-exposed placentas and may increase vascular resistance and decrease uterine blood flow.…”

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confidence: 99%

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ANKRD37 inhibits trophoblast migration and invasion by regulating the NF‐κB pathway in preeclampsia

Wang

Zhou

et al. 2022

The Journal of Gene Medicine

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Background Inadequate trophoblast invasion is associated with preeclampsia (PE). Ankyrin repeat domain protein 37 (ANKRD37) has been reported to be abnormally expressed in PE placentas. However, the role of ANKRD37 in trophoblasts has not been investigated. We aimed to determine the functions of ANKRD37 in PE and to explore the molecular mechanisms. Methods Here, fluorescence in situ hybridization, immunohistochemistry, Western blotting and quantitative real‐time polymerase chain reaction were used to detect protein and mRNA expression levels. Cell counting kit‐8 assay, 5‐ethynyl‐2′‐deoxyuridine assay, flow cytometry, wound healing assay, transwell assay and RNA sequencing were performed to investigate the role of ANKRD37 and the underlying mechanism in HTR8/SVneo and JEG‐3 cells, and extravillous explant cultures were used to evaluate the migration and invasion abilities of extravillous cytotrophoblasts. Results We found that ANKRD37 expression was upregulated in PE placentas compared to normal pregnancy placentas. ANKRD37 knockdown enhanced trophoblast migration and invasion, promoted extravillous explant outgrowth, and regulated the expression of key invasion proteins, whereas ANKRD37 overexpression exerted the opposite effects. RNA sequencing indicated that nuclear factor‐kappa B (NF‐κB) was the potential downstream pathway of ANKRD37, which was confirmed by the change in p‐p65 and p‐IκBα expression in JEG‐3 and HTR8/SVneo cells. Conclusions Our findings suggest that high expression of ANKRD37 inhibits trophoblast cell migration and invasion possibly via the NF‐κB pathway, and may be related to the development of PE.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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confidence: 99%

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ANKRD37 inhibits trophoblast migration and invasion by regulating the NF‐κB pathway in preeclampsia

Wang

Zhou

et al. 2022

The Journal of Gene Medicine

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“…Next, the cells were digested by 0.25% trypsin and centrifuged at 2,000 rpm for 5 minutes. The acquired cells were stained with annexin V-fluorescein isothiocyanate (FITC) to quantify the percentage of cells undergoing apoptosis, whereas the necrotic cells were counterstained with propidium iodide (PI) as previously described [ 19 ]. Apoptosis was analyzed using flow cytometry (BD Biosciences, Franklin Lakes, NJ, USA).…”

Section: Methodsmentioning

confidence: 99%

Fancd2os Reduces Testosterone Production by Inhibiting Steroidogenic Enzymes and Promoting Cellular Apoptosis in Murine Testicular Leydig Cells

Zhai

Wang

et al. 2022

Endocrinol Metab

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Background: It is well-established that serum testosterone in men decreases with age, yet the underlying mechanism of this change remains elusive.Methods: The expression patterns of Fancd2 opposite-strand (Fancd2os) in BALB/c male mice and testicular tissue derived cell lines (GC-1, GC-2, TM3, and TM4) were assessed using real-time polymerase chain reaction (RT-PCR), Western blot and immunofluorescence. The Fancd2os-overexpressing or knockdown TM3 cells were constructed by infecting them with lentivirus particles and were used to evaluated the function of Fancd2os. The testosterone production was measured using enzyme linked immunosorbent assay (ELISA) and the steroidogenic enzymes such as steroidogenic acute regulatory protein (StAR), P450 cholesterol side-chain cleavage (P450scc), and 3β-hydroxysteroid dehydrogenase (3β-HSD) were analysed using RT-PCR. The apoptosis of TM3 cells induced by ultraviolet light or testicular tissues was detected using flow cytometry, Western blot or dUTP-biotin nick end labeling (TUNEL) assays. Pearson correlation analysis was used to assess the correlation between the Fancd2os expression and TUNEL-positive staining in mouse testicular Leydig cells.Results: The Fancd2os protein was predominantly expressed in mouse testicular Leydig cells and its expression increased with age. Fancd2os overexpression inhibited testosterone levels in TM3 Leydig cells, whereas knockdown of Fancd2os elevated testosterone production. Fancd2os overexpression downregulated the levels of StAR, P450scc and 3β-HSD, while Fancd2os knockdown reversed this effect. Fancd2os overexpression promoted ultraviolet light-induced apoptosis of TM3 cells. In contrast, Fancd2os knockdown restrained apoptosis in TM3 cells. In vivo assays revealed that higher Fancd2os levels and mouse age were associated with increased apoptosis in Leydig cells and decreased serum testosterone levels. Pearson correlation analysis exhibited a strong positive correlation between the expression of Fancd2os and TUNEL-positive staining in mouse testicular Leydig cells.Conclusion: Our findings suggest that Fancd2os regulates testosterone synthesis via both steroidogenic enzymes and the apoptotic pathway.

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“…ANKRD49 (ankyrin repeat domain 49) contains four ankyrin motifs. ANKRD49 is highly expressed in the testes and is involved in spermatogenesis(Wang et al, 2015; Zhou et al, 2019). ANKRD49 also participates in the progression of malignant gliomas and gastric cancer in humans(Hao et al, 2017; Liu et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

ANKRD49 promotes the metastasis of NCI-H1299 and NCI-H1703 cells via activating JNK-ATF2/c-Jun-MMP-2/9 axis

Sun

Liu

et al. 2023

Preprint

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Ankyrin repeat domain 49 (ANKRD49) has been found to highly expressed in multiple cancer including lung adenocarcinoma (LUAD) and lung squamous carcinoma (LUSC). However, the function of ANKRD49 in the pathogenesis of NSCLC still remains elusive. Previously, ANKRD49 has been demonstrated to promote the invasion and metastasis of A549 cells, a LUAD cell line, via activating the p38-ATF-2-MMP2/MMP9 pathways. Considering the heterogeneity of tumor cells, the function and mechanism of ANKRD49 in NSCLC need more NSCLC-originated cells to clarify. We found that ANKRD49 promoted the migration and invasion of NCI-H1299 and NCI-H1703 cells via enhancing the levels of MMP-2 and MMP-9. Furthermore, ANKRD49 elevated phosphorylation of JNK and then activated c-Jun and ATF2 which interact in nucleus to promote the binding of ATF2:c-Jun with the promoter MMP-2 or MMP-9. In vivo assay showed that ANKRD49 promoted lung metastasis of injected-NSCLC cells and the high metastatic rate was positively correlated with the high expression of ANKRD49, MMP-2, MMP-9, p-JNK, p-c-Jun and p-ATF2. In conclusion, the present study indicated that ANKRD49 accelerated the invasion and metastasis of NSCLC cells via JNK-mediated transcription activation of c-Jun and ATF2 which regulated the expression of MMP-2/MMP-9.

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ANKRD49 inhibits etoposide-induced intrinsic apoptosis of GC-1 cells by modulating NF-κB signaling

Cited by 6 publications

References 39 publications

ANKRD37 inhibits trophoblast migration and invasion by regulating the NF‐κB pathway in preeclampsia

ANKRD37 inhibits trophoblast migration and invasion by regulating the NF‐κB pathway in preeclampsia

Fancd2os Reduces Testosterone Production by Inhibiting Steroidogenic Enzymes and Promoting Cellular Apoptosis in Murine Testicular Leydig Cells

ANKRD49 promotes the metastasis of NCI-H1299 and NCI-H1703 cells via activating JNK-ATF2/c-Jun-MMP-2/9 axis

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