Li K, Peng YF, Guo JZ, Li M, Zhang Y, Chen JY, Lin TR, Yu X, Yu WD. Abelson interactor 1 splice isoform-L plays an anti-oncogenic role in colorectal carcinoma through interactions with WAVE2 and full-length Abelson interactor 1. World J Gastroenterol 2021; 27(15): 1595-1615 [PMID: 33958846 DOI: 10.3748/wjg.v27.i15.1595]
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May 15, 2021, 13:46
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Reader Comments:
Interesting paper, revealing a new oncogenic mechanism.
Reply from the Editorial Office:
Thank you very much for your comments.
Reader's ID:
03737606
Submitted on:
April 19, 2021, 15:08
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Reader Comments:
I recognize that ABI-WAVE2 pathway has long been recognized as a pathway contributing to the adhesive and migration properties of the cells. This report referred to the role of ABI-SiL in the inhibiting effect against cell migration via hindering ABI-WAVE2 pathway and consequent function in treating metastasis of colon cancer. Therefore, the authors should pay more attention to the expression of ABI-SiL in patients with metastatic colon cancer.
In order to delineate the functions of ABI1-SiL, the authors should knockout the ABI-SiL in a cell line that expresses this isoform and observe the following change of the characteristics of the cell line.
Regarding Figure 7C and D, I am concerned that ABI1-p65 and ABI1-SiL do not bind to WAVE2 in SW480-V cells as the annotation demonstrates.
In respect of Figure 7E, I am concerned that the bidirectional co-IP and Western blot analysis did not prove the direct interaction between ABI1-SiL and ABI1-p65 as the annotation demonstrates; moreover, the co-localization between ABI1-SiL and ABI1-p65 is not a strong evidence of the interaction between these two proteins: it is possible that ABI1-SiL, ABI-p65 and WAVE2 form a complex in the cells.
In the third paragraph of Discussion, the authors misspelled “decrease” as “decresion”.
Just as discussed in the article, I am looking forward to more work about the effect of ABI1-SiL on animal experiment. Moreover, I think the authors should compare the characteristic of the tumor in which ABI1-SiL decreased with that of the tumor that ABI-SiL remained unchanged. Besides, as the isoforms share the same opening reading frame as ABI1 and the mRNA level of ABI-p65 remains the same, I am curious about the mechanism under the differential expression of the isoforms.
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