CircAMOTL1 RNA and AMOTL1 Protein: Complex Functions of AMOTL1 Gene Products

Sadlak, Joanna; Joshi, Ila; Prószyński, Tomasz J.; Kischel, Anthony

doi:10.3390/ijms24032103

Cited by 3 publications

(2 citation statements)

References 112 publications

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“…AMOTL1 is a component of tight junctions, interacting with actin to regulate cellular polarity and adhesion 37,38 . Recent studies have established a strong link between AMOTL1 and Hippo signaling pathway 39,40 . Specifically, AMOTL1 promotes the tumorigenesis via interacting with YAP1, a key factor of Hippo pathway, to induce its nuclear accumulation in gastric cancer and glioma 27,32 .…”

Section: Discussionmentioning

confidence: 99%

SRSF3/AMOTL1 Splicing Axis Promotes the Tumorigenesis of Nasopharyngeal Carcinoma through Regulating the Nucleus Translocation of YAP1

Jiang

Zhou

et al. 2023

Preprint

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Dysregulation of serine/arginine splicing factors (SRSFs) and thereby the abnormal alternative splicing (AS) has been widely implicated in the development of multiple cancers, but scarcely investigated in nasopharyngeal carcinoma (NPC). Here we examine the expression of 12 classical SRSFs between 87 NPC and 10 control samples, revealing a significant upregulation of SRSF3 and its association with worse prognosis in NPC. Functional assays demonstrate that SRSF3 exerts oncogenic function in NPC progression. Transcriptome analysis reveals 1 934 SRSF3-regulated AS events in genes involved in cell cycle and mRNA metabolism, among which generation of a long isoform of AMOTL1 (AMOTL1-L) is further verified through a direct bond of SRSF3 RRM domain with exon 12 of AMOTL1 to promote exon inclusion. Functional studies reveal that AMOTL1-L promotes proliferation and migration of NPC cells, while AMOTL1-S does not. Moreover, overexpression of AMOTL1-L significantly rescues the abovementioned inhibitory effects of SRSF3 knockdown, but not AMOTL1-S. Furthermore, compared with AMOTL1-S, AMOTL1-L has a localization preference in the intracellular than cell membrane, leading to a stronger interaction with YAP1 to promote its translocation to nucleus. Taken together, our findings identify SRSF3/AMOTL1 as a novel alternative splicing axis with pivotal roles in NPC development, which could be served as promising prognostic biomarkers and therapeutic targets of NPC.

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Section: Discussionmentioning

confidence: 99%

SRSF3/AMOTL1 Splicing Axis Promotes the Tumorigenesis of Nasopharyngeal Carcinoma through Regulating the Nucleus Translocation of YAP1

Jiang

Zhou

et al. 2023

Preprint

View full text Add to dashboard Cite

show abstract

“…AMOTL1 is a component of tight junctions, interacting with actin to regulate cellular polarity and adhesion [ 38 , 39 ]. Recent studies have established a strong link between AMOTL1 and Hippo signaling pathway [ 40 , 41 ]. Specifically, AMOTL1 promotes tumorigenesis via interacting with YAP1, a vital factor of the Hippo pathway, to induce its nuclear accumulation in gastric cancer and glioma [ 27 , 32 ].…”

Section: Discussionmentioning

confidence: 99%

SRSF3/AMOTL1 splicing axis promotes the tumorigenesis of nasopharyngeal carcinoma through regulating the nucleus translocation of YAP1

Xu,

Jiang,

Zhou

et al. 2023

Cell Death Dis

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Dysregulation of serine/arginine splicing factors (SRSFs) and abnormal alternative splicing (AS) have been widely implicated in various cancers but scarcely investigated in nasopharyngeal carcinoma (NPC). Here we examine the expression of 12 classical SRSFs between 87 NPC and 10 control samples, revealing a significant upregulation of SRSF3 and its association with worse prognosis in NPC. Functional assays demonstrate that SRSF3 exerts an oncogenic function in NPC progression. Transcriptome analysis reveals 1,934 SRSF3-regulated AS events in genes related to cell cycle and mRNA metabolism. Among these events, we verify the generation of a long isoform of AMOTL1 (AMOTL1-L) through a direct bond of the SRSF3 RRM domain with the exon 12 of AMOTL1 to promote exon inclusion. Functional studies also reveal that AMOTL1-L promotes the proliferation and migration of NPC cells, while AMOTL1-S does not. Furthermore, overexpression of AMOTL1-L, but not -S, significantly rescues the inhibitory effects of SRSF3 knockdown. Additionally, compared with AMOTL1-S, AMOTL1-L has a localization preference in the intracellular than the cell membrane, leading to a more robust interaction with YAP1 to promote nucleus translocation. Our findings identify SRSF3/AMOTL1 as a novel alternative splicing axis with pivotal roles in NPC development, which could serve as promising prognostic biomarkers and therapeutic targets for NPC.

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Hsa_circ_0001278 Facilitates Colorectal Cancer Progression via Sponging miR-338-5p and Regulating AMOTL1 Expression

Ge,

Yan,

Wang

et al. 2025

CCHTS

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Background:: Colorectal cancer (CRC) ranks as the third most common cancer and is second in terms of mortality worldwide. Circular RNAs are involved in the occurrence and development of malignant tumors by functioning either as oncogenes or tumor suppressors. Method:: This study investigated the functions of hsa_circ_0001278 in CRC. We analyzed the expression of hsa_circ_0001278 in CRC tissues and adjacent normal tissues. In order to understand the roles of hsa_circ_0001278 in CRC in terms of cellular biological behavior, in vitro experiments were conducted. A mechanistic study was designed to investigate the regulatory effect of hsa_circ_0001278 on CRC. Results:: Hsa_circ_0001278 was found to be significantly upregulated in CRC specimens. The functional analysis indicated that hsa_circ_0001278 promotes aggressive phenotypes of CRC cells. Further mechanistic studies revealed that hsa_circ_0001278 sponges miR-338-5p to regulate angiomotin-like 1 (AMOTL1), thereby facilitating CRC progression. Conclusion:: Our results demonstrate that hsa_circ_0001278 promotes malignant behaviors in CRC cells by sponging miR-338-5p to regulate AMOTL1 expression. This suggests that hsa_circ_0001278 may serve as a novel target for CRC treatment.

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CircAMOTL1 RNA and AMOTL1 Protein: Complex Functions of AMOTL1 Gene Products

Cited by 3 publications

References 112 publications

SRSF3/AMOTL1 Splicing Axis Promotes the Tumorigenesis of Nasopharyngeal Carcinoma through Regulating the Nucleus Translocation of YAP1

SRSF3/AMOTL1 Splicing Axis Promotes the Tumorigenesis of Nasopharyngeal Carcinoma through Regulating the Nucleus Translocation of YAP1

SRSF3/AMOTL1 splicing axis promotes the tumorigenesis of nasopharyngeal carcinoma through regulating the nucleus translocation of YAP1

Hsa_circ_0001278 Facilitates Colorectal Cancer Progression via Sponging miR-338-5p and Regulating AMOTL1 Expression

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