HILI destabilizes microtubules by suppressing phosphorylation and Gigaxonin-mediated degradation of TBCB

Tan, Hao; Liao, Huimin; Zhao, Lianfang; Lu, Yilu; Jiang, Siyuan; Tao, Dachang; Ma, Yongxin

doi:10.1038/srep46376

Cited by 11 publications

(11 citation statements)

References 40 publications

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“…HeLa and HepG2 cells used in this research were conserved in our laboratory as previously described 18 , 19 . They were grown in Dulbecco’s modified Eagle’s medium with 5% fetal bovine serum (FBS, HyClone, USA) cultured in a humidified incubator (at 37 °C, 5% CO 2 ) before transfection was performed, and the medium was changed every other day.…”

Section: Methodsmentioning

confidence: 99%

CLOCK and BMAL1 stabilize and activate RHOA to promote F-actin formation in cancer cells

Zhang

et al. 2018

Exp Mol Med

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Circadian genes control most of the physiological functions in cancer cells, including cell proliferation, migration, and invasion. The CLOCK and BMAL1 complex plays a central role in circadian rhythms. Previous studies have shown that circadian genes may act as oncogenes or tumor-suppressor genes. In addition, F-actin, regulated by RHOA, has been shown to participate in tumor progression. However, the roles of the CLOCK and BMAL1 genes in the regulation of tumor progression via the RHOA-ROCK-CFL pathway remain largely unclear. Here we first indicate that the rearrangement of F-actin is regulated by CLOCK and BMAL1. We found that CLOCK and BMAL1 can upregulate RHOA expression by inhibiting CUL3-mediated ubiquitination and activate RHOA by reducing the interaction between RHOA and RhoGDI. Consequently, CLOCK and BMAL1 control the expression of the components of the RHOA-ROCK-CFL pathway, which alters the dynamics of F-actin/G-actin turnover and promotes cancer cell proliferation, migration, and invasion. In conclusion, our research proposes a novel insight into the role of CLOCK and BMAL1 in tumor cells.

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Section: Methodsmentioning

confidence: 99%

CLOCK and BMAL1 stabilize and activate RHOA to promote F-actin formation in cancer cells

Zhang

et al. 2018

Exp Mol Med

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“…In prostate cancer, PIWIL2 overexpression was associated with deregulation of EMT factors. In breast cancer, PIWIL2 and piRNA 932 overexpression promoted EMT in CD44+/ CD24− CSCs [31].…”

Section: Emt Invasion and Metastasismentioning

confidence: 98%

“…Direct interaction between Stathmin1 and PIWIL1 prevented its inhibition by CaMKII and its degradation by E3 ubiquitin ligase RLIM. PIWIL2 promoted interaction of the tubulin folding cofactor B (TBCB) with HSP90 and repressed binding of TBCB to the E3 ubiquitin ligase adaptor protein gigaxonin, resulting in tubulin polymerization and microtubule edification during cell division [31].…”

Section: Proliferation Apoptosis and Stemnessmentioning

confidence: 99%

“…In breast cancer, piR-4987 upregulation was significantly associated with lymph node metastasis and PIWIL2-piR-932 complex enhanced EMT through Latexin methylation of its promoter region [31,48,49]. In clear cell renal cell carcinoma, 19 piRNAs were differentially expressed between tumor and normal tissues and 46 piRNAs were associated with metastasis and poor survival [43].…”

Section: Invasion and Metastatic Spreadmentioning

confidence: 99%

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Part 2: Deregulated Expressions of PIWI Proteins and piRNAs as New Candidate Biomarkers and Potential Therapeutic Tools in Cancer

Meseure¹,

Alsibai²

2020

Chromatin and Epigenetics

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Epigenetic abnormalities are early events in carcinogenesis and associate heterogeneity of DNA methylation, modifications of histones, and deregulation of noncoding RNAs. Aberrant expressions of PIWI proteins and piRNAs were recently observed in numerous subtypes of malignant tumors and were implicated in occurrence of most cancer hallmarks such as cell proliferation, genomic stability, apoptosis inhibition, invasion, and metastatic spread. However, this pathway is a new emerging research field, and further investigations are necessary to elucidate their oncogenic or tumor-suppressing status. Since the aberrant expression of this pathway may induce stemness, analysis of relationship between PIWI proteins, piRNAs, and cancer stem cells may open new avenues in cancer research. The objective of this review is to provide a broad overview of the emerging implication of PIWI proteins and piRNAs in carcinogenesis and their potential clinical interest as diagnostic and prognostic biomarkers and therapeutic tools.

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“…The results presented above indicate that TBCB may interact with and be modified by SseK1, opening the possibility that this Salmonella effector may have an impact on microtubule dynamics. To test this hypothesis, we transfected HEK293T cells with plasmids expressing GFP-SseK1 or GFP alone, and we measured the acetylation level of α-tubulin by fluorescence microscopy since acetylation of α-tubulin correlates with microtubule stability [19][20][21]. The expression of SseK1 significantly increased the level of acetylated microtubules (Figure 7).…”

Section: Ssek1 Promotes Microtubule Stabilitymentioning

confidence: 99%

Tubulin Folding Cofactor TBCB is a Target of the Salmonella Effector Protein SseK1

Araujo-Garrido

Baisón-Olmo

Bernal-Bayard

et al. 2020

IJMS

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Salmonella enterica serovar Typhimurium is a human and animal pathogen that uses type III secretion system effectors to manipulate the host cell and fulfill infection. SseK1 is a Salmonella effector with glycosyltransferase activity. We carried out a yeast two-hybrid screen and have identified tubulin-binding cofactor B (TBCB) as a new binding partner for this effector. SseK1 catalyzed the addition of N-acetylglucosamine to arginine on TBCB, and its expression promoted the stabilization of the microtubule cytoskeleton of HEK293T cells. The conserved Asp-x-Asp (DxD) motif that is essential for the activity of SseK1 was required for the binding and modification of TBCB and for the effect on the cytoskeleton. Our study has identified a novel target for SseK1 and suggests that this effector may have a role in the manipulation of the host cell microtubule network to provide a safe niche for this pathogen.

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HILI destabilizes microtubules by suppressing phosphorylation and Gigaxonin-mediated degradation of TBCB

Cited by 11 publications

References 40 publications

CLOCK and BMAL1 stabilize and activate RHOA to promote F-actin formation in cancer cells

CLOCK and BMAL1 stabilize and activate RHOA to promote F-actin formation in cancer cells

Part 2: Deregulated Expressions of PIWI Proteins and piRNAs as New Candidate Biomarkers and Potential Therapeutic Tools in Cancer

Tubulin Folding Cofactor TBCB is a Target of the Salmonella Effector Protein SseK1

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