Correction to “Alternative RNA Splicing of the GIT1 Gene Is Associated With Neuroendocrine Prostate Cancer”

IF 4.3 2区 医学 Q1 ONCOLOGY
Cancer Science Pub Date : 2025-07-09 DOI:10.1111/cas.70140
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引用次数: 0

Abstract

A. R. Lee, Y. Gan, N. Xie, V. R. Ramnarine, J. M. Lovnicki, and X. Dong, “Alternative RNA Splicing of the GIT1 Gene Is Associated With Neuroendocrine Prostate Cancer,” Cancer Science 110, no. 1 (2019): 245–255, https://doi.org/10.1111/cas.13869.

Concerns were raised by a third party regarding image panels with insets without any magnification or scale bar in Figure 2A. The authors acknowledged that these insets were cropped and amplified from the original images; therefore, no scale bar was inserted. The unamplified insets were replaced by the 10× magnified panels accordingly.

The corrected Figure 2A and its corrected figure caption are as follows:

Figure 2

RNA splicing of GIT1 is associated with clinical NEPC tumors. A, RISH probes targeting the exons 7/8 or exons 7/9 junction were created to detect GIT1-A or GIT1-C, respectively, in a human CRPC TMA (n = 64 cores). TMA was stained against CHGA, SYP, CD56, AR, and PSA by immunohistochemistry (IHC). Columns in the heatmap represent one of 64 cores. One representative core from each of the histologically diagnosed AdPC (n = 52), AdNC (n = 6), and SCNC (n = 6) cores is shown. Scale bars represent 25 μm. Insets represent cropped and 10× amplified images.

In addition, the figure captions of Figures 3A and 5 have also been revised, as follows:

Figure 3

SRRM4 regulates RNA splicing of GIT1. A, Matched TMA cores are shown to represent the associations of the expressions of SRRM4 with GIT1-A and GIT1-C. Scale bars represent 25 μm. Insets represent cropped and 10× amplified images.

Figure 5

Differential functions of the GIT1 splice variants in FA stability. DU145 stable cell lines overexpressing GIT1-A, GIT1-C, or empty vector were seeded on coverslips and serum-starved. They were treated with 10 μmol/L nocodazole for 4 h, subsequently washed away, and replaced with serum-containing medium. Cells were fixed at 0 or 120 min after the washout, costained against GIT1 and vinculin, and then mounted with DAPI staining mount. Cells were imaged using a Zeiss AxioObserver Z1 (Carl Zeiss AG; Oberkochen, Germany) microscope, where the scale bar represents 10 μm. Insets represent cropped and 10× amplified images. Arrowheads indicate FA complexes. Overlapping signals between GIT1 and vinculin appear yellow. Overlapping of the two signals in a cross section (indicated by white line) of FA complexes was profiled by the ZEN program. All experiments were repeated three times. FA, focal adhesion; GIT1, G-protein-coupled receptor kinase-interacting protein 1; IF, immunofluorescence; ZEN, ZEISS efficient navigation.

Abstract Image

更正“GIT1基因的选择性RNA剪接与神经内分泌前列腺癌有关”。
李亚荣,甘艳,谢楠,董晓霞,“GIT1基因的选择性剪接与神经内分泌前列腺癌的关系”,中国癌症杂志,第11期。1 (2019): 245-255, https://doi.org/10.1111/cas.13869.Concerns由第三方就图2A中没有任何放大或比例尺的插页图像面板提出。作者承认,这些插图是从原始图像中裁剪和放大的;因此,没有插入比例尺。未放大的插页相应地被放大10倍的面板所取代。图2 GIT1的RNA剪接与临床NEPC肿瘤相关。A、RISH探针针对外显子7/8或外显子7/9连接分别检测人CRPC TMA (n = 64个核)中的GIT1-A或GIT1-C。采用免疫组化(IHC)对TMA进行CHGA、SYP、CD56、AR和PSA染色。热图中的列表示64个核心中的一个。图中显示了组织学诊断为AdPC (n = 52)、AdNC (n = 6)和SCNC (n = 6)的代表性核心。比例尺代表25 μm。插页表示裁剪和10倍放大的图像。此外,对图3A和图5的标题也进行了修改,如下图所示:图3 SRRM4调控GIT1的RNA剪接。A,匹配的TMA核心显示了SRRM4与GIT1-A和GIT1-C表达的关联。比例尺代表25 μm。插页表示裁剪和10倍放大的图像。图5 GIT1剪接变异体在FA稳定性中的微分函数。将过表达GIT1-A、GIT1-C或空载体的DU145稳定细胞系接种于盖片上并进行血清饥饿。10 μmol/L诺可唑处理4 h后洗净,用含血清培养基代替。冲洗后0或120min固定细胞,分别对GIT1和vinculin进行染色,然后用DAPI染色载具进行载药。使用Zeiss AxioObserver Z1 (Carl Zeiss AG; Oberkochen, Germany)显微镜对细胞进行成像,其中比尺为10 μm。插页表示裁剪和10倍放大的图像。箭头表示FA复合物。GIT1和血管蛋白之间的重叠信号呈黄色。两个信号在FA配合物的横截面(用白线表示)上的重叠被ZEN程序描述。所有实验重复三次。FA, focal adhesion;GIT1, g蛋白偶联受体激酶相互作用蛋白1;如果,免疫荧光;ZEN,蔡司高效导航。
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来源期刊
Cancer Science
Cancer Science 医学-肿瘤学
自引率
3.50%
发文量
406
审稿时长
2 months
期刊介绍: Cancer Science (formerly Japanese Journal of Cancer Research) is a monthly publication of the Japanese Cancer Association. First published in 1907, the Journal continues to publish original articles, editorials, and letters to the editor, describing original research in the fields of basic, translational and clinical cancer research. The Journal also accepts reports and case reports. Cancer Science aims to present highly significant and timely findings that have a significant clinical impact on oncologists or that may alter the disease concept of a tumor. The Journal will not publish case reports that describe a rare tumor or condition without new findings to be added to previous reports; combination of different tumors without new suggestive findings for oncological research; remarkable effect of already known treatments without suggestive data to explain the exceptional result. Review articles may also be published.
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