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Table 1 Functional role of AMOT, AMOTL1, and AMOTL2 in different cancer types

From: The physiological role of Motin family and its dysregulation in tumorigenesis



Cancer type






A DNA vaccine targeting AMOT inhibits angiogenesis and suppresses tumor growth. Therapeutic antibodies targeting AMOT inhibit angiogenesis in vivo. A vaccine targeting AMOT hampers tumor growth. sCD146 binds to Amot to stimulate a proangiogenic response. Tankyrase inhibitors antagonizes stabilize AMOT and result in constitutive activates of TEAD-dependent transcription and proliferation of human tumor cells

[29, 62, 79,80,81]

Breast cancer

AMOT is up-regulated and its expression links to the aggressive nature of breast cancer. It promotes breast cancer cell proliferation and invasion. AMOT increases the expression of YAP1 in the nucleoprotein. miR-205 inhibits the proliferation and invasion of breast cancer by regulating AMOT expression

[71, 78, 89]

Sinonasal inverted papilloma

AMOT is over-expressed. It associates with progression and growth via promoting angiogenesis in sinonasal inverted papilloma



lncRNA SNHG12 promotes cell proliferation and migration by activating AMOT gene expression. Also, miR-497 inhibits cell proliferation, migration, and invasion by targeting AMOT

[87, 88]

Renal cell carcinoma

AMOT promotes cell proliferation by retaining the nuclear YAP1


Colon cancer

AMOT promotes the malignant potential of colon cancer cells by activating the YAP1-ERK/PI3 K-AKT signaling pathway


Tumor suppressor


Form a TJ-associated protein complex with Merlin, Patj, and Pals1. AMOT inhibits MAPK signaling. AMOT inhibits YAP1 oncoprotein and restricts the activity of YAP1/TAZ. AMOT activates LATS2. Tankyrase inhibitors stabilize AMOT family proteins and suppress YAP1 oncogenic functions. Deubiquitylation of AMOT at lysine 496 by USP9x resulting in stabilization of AMOT and lower YAP1/TAZ activity

[6, 48, 55, 61, 65, 98]

Lung cancer

AMOT decreases lung cancer progression by sequestering oncogenic YAP1/TAZ and decreasing Cyr61 expression. Tankyrase inhibitor sensitizes lung cancer cells to endothelial growth factor receptor inhibition via stabilizing AMOT and inhibiting YAP1 signaling

[59, 60]




AMOT-p80 promotes angiogenesis by stimulating invasion and stabilizing established tubes


Head and neck squamous cell carcinoma

High expression AMOT-p80 promotes cell proliferation and migration


Prostate cancer

AMOT-p80 is a novel component of cadherin-11/β-catenin/p120 complex and promotes cell migration





AMOT-p130 acts as a YAP1 cofactor, preventing YAP1 phosphorylation and augmenting its activity


Tumor suppressor


AMOT-p130 and AIP4 cooperatively reduces YAP1 and cell growth. AMOT-p130 selectively induced YAP1 phosphorylation and reduced transcription of connective tissue growth factor in an AIP4-dependent manner. AMOT-p130 decreased the growth of MDA-MB-468 breast cancer cells. AMOT-p130 (S175A)-expressing cells formed enlarged and poorly differentiated acini

[64, 66]



Breast cancer

AMOTL1 marginally expressed higher levels in tumor than normal tissues. AMOTL1 promotes breast cancer progression and is antagonized by Merlin. AMOTL1 is an essential effector of the N-cadherin mediated endothelial/pericyte junctional complex

[39, 78, 99]

Cervical cancer

MiR-124 represses vasculogenic mimicry and cell motility by targeting AMOTL1


Tumor suppressor


AMOTL1 activates LATS2, inhibits YAP1, and restricts the activity of TAZ and YAP1. It inhibits YAP1′s nuclear translocation and pro-apoptotic function

[51, 52, 55, 65, 69]




AMOTL2 promotes cell migration and proliferation of angiogenic endothelial cells. It positively regulates MAPK/ERK activation


Breast cancer

AMOTL2 marginally expressed higher in tumors. It disrupts apical–basal cell polarity and promotes tumor invasion

[78, 90]

Tumor suppressor


AMOTL2 regulates YAP1 cytoplasm-to-nucleus translocation. AMOTL2 inhibits epithelial-mesenchymal transition. LATS2, AMOTL2, and YAP1 all localize to TJs, trigger LATS2 activation and growth inhibition in response to increased cell density. AMOTL2 mono-ubiquitination is required for YAP1 inhibition

[54, 65, 69]


mTORC2/AMOTL2/YAP1 signaling cascade promotes glioblastoma growth and invasive characteristics. AMOTL2 upregulation inhibited YAP1-induced transcription, foci formation, growth, and metastatic properties both in vitro and in vivo