Correction: CMTM6 overexpression confers trastuzumab resistance in HER2‑positive breast cancer

Abstract

Correction: Mol Cancer 22, 6 (2023)

https://doi.org/10.1186/s12943-023–01716-y

Following publication of the original article [1], the authors sincerely acknowledge that an incorrect image panel was inadvertently included in Figure 3F and 4H. To ensure the accuracy and integrity of the article, the authors have carefully reviewed the original data and replaced the erroneous images. This correction does not affect the main findings or conclusions of the study. The revised figures and their corresponding correct captions are provided below.

Incorrect Fig. 3 and incorrect caption:

Fig. 3

CMTM6 promotes the survival, migration, invasion and trastuzumab resistance of BC cells in vitro. A qRT-PCR and Western blot validated CMTM6 silencing in JIMT-1 cells and CMTM6-overexpresstion in SKBR3 cells. Negative control (NC) JIMT-1 and SKBR3 cells were transduced with lentivirus for the control shRNA or transfected with the control plasmid, respectively. B, C CCK-8 assay determined the viability of the indicated BC cells following treatment with trastuzumab (0–100 μg/ml). D, E ethynyl-2′-deoxyuridine (EdU) analysis of the proliferation of CMTM6-silenced JIMT-1 cells, CMTM6 overexpressing SKBR3 cells, control JIMT-1 cells and SKBR3 cells following treatment with trastuzumab (10 μg/ml). (scale bar, 50 μM). F, G TUNEL analysis of apoptotic CMTM6-silenced JIMT-1 cells, CMTM6 overexpressing SKBR3 cells, control JIMT-1 and SKBR3 cells following treatment with trastuzumab (10 μg/ml). H, I Cell invasion assay revealed that CMTM6 silencing inhibited JIMT-1 cell invasion while CMTM6 overexpression enhanced SKBR3 cell invasion following treatment with trastuzumab (10 μg/ml). (scale bar, 50 μM). Data are representative images or expressed as the mean ± SD of each group from three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001

Full size image

Correct Fig. 3 and correct caption:

Fig. 3

CMTM6 promotes the survival, migration, invasion and trastuzumab resistance of BC cells in vitro. A qRT-PCR and Western blot validated CMTM6 silencing in JIMT-1 cells and CMTM6-overexpresstion in SKBR3 cells. Negative control (NC) JIMT-1 and SKBR3 cells were transduced with lentivirus for the control shRNA or transfected with the control plasmid, respectively. B, C CCK-8 assay determined the viability of the indicated BC cells following treatment with trastuzumab (0–100 μg/ml). D, E ethynyl-2′-deoxyuridine (EdU) analysis of the proliferation of CMTM6-silenced JIMT-1 cells, CMTM6 overexpressing SKBR3 cells, control JIMT-1 cells and SKBR3 cells following treatment with trastuzumab (10 μg/ml). (scale bar, 50 μM). F, G TUNEL analysis of apoptotic CMTM6-silenced JIMT-1 cells and control JIMT-1 cells following treatment with trastuzumab (10 μg/ml). H, I Cell invasion assay revealed that CMTM6 silencing inhibited JIMT-1 cell invasion while CMTM6 overexpression enhanced SKBR3 cell invasion following treatment with trastuzumab (10 μg/ml). (scale bar, 50 μM). Data are representative images or expressed as the mean ± SD of each group from three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001

Full size image

Incorrect Fig. 4 and incorrect caption:

Fig. 4

CMTM6 directly interacts with HER2 and enhancing the HER2 signaling in BC cells. A IHC analysis of HER2 protein expression in BC tissues with low or high CMTM6 protein expression (scale bar, 50 μM). B Association between CMTM6 and HER2 protein expression in BC tissues. C Western blot analysis of CMTM6 and HER2 protein levels in BC tissues. D Correlation between CMTM6 and HER2 protein levels in BC tissues. Data are mean ± SEM. E Confocal microscopy analysis of the subcellular co-localization of CMTM6 (green) and HER2 (red) in JIMT-1 cells, with DAPI nuclear staining (blue) (scale bar, 10 μM). F, G Co-immunoprecipitation revealed the direct interaction between endogenous CMTM6 and HER2 proteins in JIMT-1 cells. H Western blot analysis of CMTM6, HER2, p-HER2, PI3K, AKT, MEK, ERK, N-cadherin and E-cadherin protein levels in CMTM6-silenced JIMT-1, CMTM6 overexpressing SKBR3, control JIMT-1 and SKBR3 cells. Data are representative images of each group of cells from three separate experiments

Full size image

Correct Fig. 4 and correct caption:

Fig. 4

CMTM6 directly interacts with HER2 and enhancing the HER2 signaling in BC cells. A IHC analysis of HER2 protein expression in BC tissues with low or high CMTM6 protein expression (scale bar, 50 μM). B Association between CMTM6 and HER2 protein expression in BC tissues. C Western blot analysis of CMTM6 and HER2 protein levels in BC tissues. D Correlation between CMTM6 and HER2 protein levels in BC tissues. Data are mean ± SEM. E Confocal microscopy analysis of the subcellular co-localization of CMTM6 (green) and HER2 (red) in JIMT-1 cells, with DAPI nuclear staining (blue) (scale bar, 10 μM). F, G Co-immunoprecipitation revealed the direct interaction between endogenous CMTM6 and HER2 proteins in JIMT-1 cells. H Western blot analysis of CMTM6, HER2, p-HER2, PI3K, AKT, MEK, ERK, N-cadherin, and E-cadherin protein levels in CMTM6-silenced JIMT-1, CMTM6 overexpressing SKBR3, control JIMT-1 and SKBR3 cells. Data are representative images of each group of cells from three separate experiments.

Full size image

1. Xing F, Gao H, Chen G, et al. CMTM6 overexpression confers trastuzumab resistance in HER2-positive breast cancer. Mol Cancer. 2023;22:6. https://doi.org/10.1186/s12943-023-01716-y.

   Article CAS PubMed PubMed Central Google Scholar

Download references

Authors and Affiliations

1. Department of Oncology, Innovative Cancer Drug Research and Engineering Center of Liaoning Province, Cancer Stem Cell and Translation Medicine Lab, Shengjing Hospital of China Medical University, Shenyang, 110022, China

   Fei Xing, Hongli Gao, Guanglei Chen, Lisha Sun, Jiayi Sun, Xinbo Qiao, Jinqi Xue & Caigang Liu

Authors

1. Fei XingView author publications

   You can also search for this author inPubMed Google Scholar

2. Hongli GaoView author publications

   You can also search for this author inPubMed Google Scholar

3. Guanglei ChenView author publications

   You can also search for this author inPubMed Google Scholar

4. Lisha SunView author publications

   You can also search for this author inPubMed Google Scholar

5. Jiayi SunView author publications

   You can also search for this author inPubMed Google Scholar

6. Xinbo QiaoView author publications

   You can also search for this author inPubMed Google Scholar

7. Jinqi XueView author publications

   You can also search for this author inPubMed Google Scholar

8. Caigang LiuView author publications

   You can also search for this author inPubMed Google Scholar

Corresponding author

Correspondence to Caigang Liu.

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.

Reprints and permissions

Cite this article

Xing, F., Gao, H., Chen, G. et al. Correction: CMTM6 overexpression confers trastuzumab resistance in HER2‑positive breast cancer. Mol Cancer 24, 115 (2025). https://doi.org/10.1186/s12943-025-02317-7

Download citation

• Published: 14 April 2025

• DOI: https://doi.org/10.1186/s12943-025-02317-7

Share this article

Anyone you share the following link with will be able to read this content:

Get shareable link

Sorry, a shareable link is not currently available for this article.

Copy to clipboard

Provided by the Springer Nature SharedIt content-sharing initiative