ADCK1 activates the β-catenin/TCF signaling pathway to promote the growth and migration of colon cancer cells

Ji, Yong; Sun, Changchun; Yu, Lijiang; Wang, Zhao; Du, Xuhua; Wu, Yang; Zhang, Chenggong; Tao, Chunmu; Wang, Jianjiang; Yang, Xi; Sun, Da; Huang, Yu‐Feng

doi:10.1038/s41419-021-03624-9

Cited by 2 publications

(4 citation statements)

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“…The lentiviral particles encoding the ADCK1 shRNA (sequence listed in [ 16 ]), the ADCK2 shRNA, the ADCK3 shRNA, or the mTOR shRNA were obtained from GeneChem Inc. (Shanghai, China). According to the instruction, OS were plated into a six-well plate at 8.5 × 10 4 cells per well for 24 h. Cells were then infected with the virus at the multiplicity of infection (MOI) of 20.…”

Section: Methodsmentioning

confidence: 99%

“…It is not clear whether ADCK1 also affects the functions of mitochondria and behaviors of human cells, and whether its expression is altered in human cancer cells. A very recent study by Ji et al, reported that ADCK1 is overexpressed in clinical colon cancer specimens and involved in colon cancer tumorigenesis [ 16 ]. ADCK1 silencing, by the shRNA strategy, potently inhibited colon cancer cell colony formation and infiltration as well as the in vivo tumorigenesis, migration, and organoid formation [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

“…A very recent study by Ji et al, reported that ADCK1 is overexpressed in clinical colon cancer specimens and involved in colon cancer tumorigenesis [ 16 ]. ADCK1 silencing, by the shRNA strategy, potently inhibited colon cancer cell colony formation and infiltration as well as the in vivo tumorigenesis, migration, and organoid formation [ 16 ]. ADCK1 directly associated with TCF4 (T-cell factor 4) to activate the β-catenin/TCF signaling pathway, thus promoting expression of β-catenin downstream genes [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

“…ADCK1 silencing, by the shRNA strategy, potently inhibited colon cancer cell colony formation and infiltration as well as the in vivo tumorigenesis, migration, and organoid formation [ 16 ]. ADCK1 directly associated with TCF4 (T-cell factor 4) to activate the β-catenin/TCF signaling pathway, thus promoting expression of β-catenin downstream genes [ 16 ]. Its expression and potential functions in OS are examined in the present study.…”

Section: Introductionmentioning

confidence: 99%

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ADCK1 is a potential therapeutic target of osteosarcoma

et al. 2022

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We here showed that ADCK1 (AarF domain-containing kinase 1), a mitochondrial protein, is upregulated in human osteosarcoma (OS) tissues and OS cells. In primary and established OS cells, ADCK1 shRNA or CRISPR/Cas9-induced ADCK1 knockout (KO) remarkably inhibited cell viability, proliferation and migration, and provoked apoptosis activation. Conversely, ectopic ADCK1 overexpression exerted pro-cancerous activity by promoting OS cell proliferation and migration. ADCK1 depletion disrupted mitochondrial functions in OS cells and induced mitochondrial membrane potential reduction, ATP depletion, reactive oxygen species production. Significantly, ADCK1 silencing augmented doxorubicin-induced apoptosis in primary OS cells. mTOR activation is important for ADCK1 expression in OS cells. The mTOR inhibitors, rapamycin and AZD2014, as well as mTOR shRNA, potently decreased ADCK1 expression in primary OS cells. In nude mice, the growth of subcutaneous pOS-1 xenografts was largely inhibited when bearing ADCK1 shRNA or ADCK1 KO construct. Moreover, ADCK1 KO largely inhibited pOS-1 xenograft in situ growth in proximal tibia of nude mice. ADCK1 depletion, apoptosis activation and ATP reduction were detected in pOS-1 xenografts bearing ADCK1 shRNA or ADCK1 KO construct. Together, the mitochondrial protein ADCK1 is required for OS cell growth and is a novel therapeutic target of OS.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%