The Drosophila DOCK family protein Sponge is required for development of the air sac primordium

Morishita, Kazushge; Suong, Dang Ngoc Anh; Yoshida, Hideki; Yamaguchi, Masamitsu

doi:10.1016/j.yexcr.2017.03.044

Cited by 4 publications

(6 citation statements)

References 42 publications

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“…Our previous studies in Drosophila revealed that the DOCK-B protein, Spg positively regulates ERK pathway to control the differentiation of R7 photoreceptor cells and air sac development (Eguchi et al, 2013;Morishita et al, 2017). Spg also activates JNK pathway to promote thorax development (Morishita et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

“…Duolink in situ PLA method using specific antibodies to Spg and Rap1 revealed that this positive regulation is mediated by interaction of Spg with Rap1. Spg also plays a critical role in ASP development and tracheal cell viability that is mediated by the ERK signaling pathway (Morishita et al, 2017). In contrast, during thorax development, Spg positively regulates JNK pathway and this regulation is mediated by its association with Rac1 (Morishita et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

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<i>Drosophila</i> DOCK Family Protein Zizimin Involves in Pigment Cell Differentiation in Pupal Retinae

Ozasa

Morishita

Dang

et al. 2017

Cell Struct. Funct.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

<i>Drosophila</i> DOCK Family Protein Zizimin Involves in Pigment Cell Differentiation in Pupal Retinae

Ozasa

Morishita

Dang

et al. 2017

Cell Struct. Funct.

Self Cite

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“…Recently, the Drosophila ortholog of dedicator of cytokinesis (DOCK) family proteins 3 and 4 (DOCK3/4), sponge (Spg), was reported to promote cell survival through MAPK signaling as well. The authors of the study suggest that this could be accomplished via the intermediate activation of p21-activated kinase (PAK), but this model currently lacks experimental evidence [ 63 ].…”

Section: Additional Regulators Of Asp Developmentmentioning

confidence: 99%

The Air Sac Primordium of Drosophila: A Model for Invasive Development

Powers

Srivastava

2018

IJMS

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The acquisition of invasive properties preceding tumor metastasis is critical for cancer progression. This phenomenon may result from mutagenic disruption of typical cell function, but recent evidence suggests that cancer cells frequently co-opt normal developmental programs to facilitate invasion as well. The signaling cascades that have been implicated present an obstacle to identifying effective therapeutic targets because of their complex nature and modulatory capacity through crosstalk with other pathways. Substantial efforts have been made to study invasive behavior during organogenesis in several organisms, but another model found in Drosophila melanogaster has not been thoroughly explored. The air sac primordium (ASP) appears to be a suitable candidate for investigating the genes and morphogens required for invasion due to the distinct overlap in the events that occur during its normal growth and the development of metastatic tumor cells. Among these events are the conversion of larval cells in the trachea into a population of mitotically active cells, reduced cell–cell contact along the leading edge of the ASP, and remodeling of the extracellular matrix (ECM) that surrounds the structure. Here, we summarize the development of ASPs and invasive behavior observed therein.

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“…The dedicator of cytokinesis (docK) family is one of the two members of the RAC guanine nucleotide exchange factor (GeF) family, which contain the evolutionarily conserved lipid-binding DOCK homology region-1 (DHR-1) domain and the catalytic dHr-2 domain (8). as a rac-specific GEF, DOCK1 regulates phagocytosis, myoblastic fusion, cell migration and circular dorsal fold formation (9,10). Abnormal expression and activity of DOCK1 is associated with the malignant characteristics of multiple tumors (11)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

TBOPP enhances the anticancer effect of cisplatin by inhibiting DOCK1 in renal cell carcinoma

et al. 2020

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The treatment of renal cell carcinoma (rcc) with chemotherapy remains a challenge; therefore, improving the knowledge of the molecular mechanisms underlying rcc chemoresistance and developing novel therapeutic strategies is important. Dedicator of cytokinesis 1 (DOCK1), the first member of the DOCK family to be discovered, displays various roles during tumorigenesis; however, its role during rcc progression is not completely understood. Therefore, the present study aimed to clarify the function of DOCK1 and 1-[2-(3'-(trifluorom ethyl)-(1,1'-biphenyl)-4-yl)-2-oxoethyl]-5-pyrrolidinylsulfonyl-2 (1H)-pyridone (TBOPP), a DOCK1-sensitive inhibitor, during rcc development and chemoresistance. The results of ccK-8 and edu assay indicated that TBoPP decreased rcc cell viability and proliferation compared with the control group, and sensitized rcc cells to cisplatin. Moreover, rcc cells with high DOCK1 expression levels displayed increased resistance to cisplatin, whereas docK1 knockdown enhanced the lethal effects of cisplatin on rcc cells. Furthermore, the results determined by western blotting, CCK-8 and cell apoptosis assay indicated that TBoPP effectively reduced docK1 expression levels compared with the control group, and the TBOPP-mediated cisplatin sensitizing effect was mediated by DOCK1 inhibition. The present study suggests that DOCK1 plays a vital role in rcc cell chemoresistance to cisplatin; therefore, TBoPP may serve as a novel therapeutic agent for rcc chemoresistance.

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The Drosophila DOCK family protein Sponge is required for development of the air sac primordium

Cited by 4 publications

References 42 publications

<i>Drosophila</i> DOCK Family Protein Zizimin Involves in Pigment Cell Differentiation in Pupal Retinae

<i>Drosophila</i> DOCK Family Protein Zizimin Involves in Pigment Cell Differentiation in Pupal Retinae

The Air Sac Primordium of Drosophila: A Model for Invasive Development

TBOPP enhances the anticancer effect of cisplatin by inhibiting DOCK1 in renal cell carcinoma

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