Erratum to hypofractionation in prostate cancer radiotherapy
Erratum

Erratum to hypofractionation in prostate cancer radiotherapy

Editorial Office

Translational Cancer Research

Correspondence to: Editorial Office. Translational Cancer Research. Email: tcr@amepc.org.

Submitted Oct 09, 2023. Accepted for publication Dec 12, 2023. Published online Jan 24, 2024.

doi: 10.21037/tcr-2023-09


Erratum to: Transl Cancer Res 2020;9:763-73.

In the February 2020 issue of Translational Cancer Research, the paper titled “High-mobility group A1 (HMGA1) gene expressions in various colorectal cancer cell lines and correlation with prognosis” (1), was published with some errors in Figure 4D and the description of the Figure 4 in the “Results” section. The reason is that the scatterplot is incorrectly named.

Figure 4 High expression of HMGA1 in kidney correlated with worse overall survival. (A) Kaplan-Meier analysis of HMGA1 expression level in kidney papillary cell carcinoma patients; (B) Scatter plot of HMGA1 in matched normal and kidney papillary cell carcinoma tissues; (C) Kaplan-Meier analysis of HMGA1 expression level in kidney clear cell carcinoma patients; (D) Scatter plot of HMGA1 in matched normal and kidney clear cell carcinoma tissues. ***, P<0.001. TCGA, The Cancer Genome Atlas.

In the “Results” section, the description of the Figure 4 and the whole Figure 4 should be corrected as below (the figure legend remains intact):


Results

Expression levels of HMGA1 in kidney cancer (RCC) (Figure 4)

We analyzed the HMGA1 expression level in kidney papillary cell carcinoma (pRCC) and kidney clear cell carcinoma (ccRCC). We found that HMGA1 expression level correlated with the clinical overall survival time of patients. The data showed that the lower expression HMGA1 group had a significantly higher (P<0.05) ten-year survival rate than the high expression group (Figure 4A,4C). We also analyzed the expression level of HMGA1 in kidney tumor tissues and matched normal tissues; the analysis indicated a high expression of HMGA1 in pRCC tissues in contrast to normal tissues (P<0.05) (Figure 4B). Conversely, ccRCC displayed an opposing pattern (Figure 4D). Emerging evidence suggests that HMGA1 is higher expressed in ccRCC tissues than normal tissues, especially in metastatic tumor tissues and high-grade RCC (13-16), Chi et al. identified HMGA1 have promote the metastasis of ccRCC via Wnt signaling pathways (17). Several factors might explain the observed reduced HMGA1 expression in our ccRCC: (I) potential limitations in enrollment within TCGA database, possibly influenced by population biases and a constrained patient cohort (18); (II) the scatter plot delineates the disparities in gene expression between cancer and normal tissues, primarily reflecting the variations arising during tumorigenesis. Concurrently, survival prognosis analysis stratifies HMGA1 gene expression in cancer tissues into higher and lower cohorts, subsequently investigating the implications of HMGA1 in the malignancy progression. Notably, RCC exhibits a comparatively favorable prognosis, The 5-year survival of RCC patients with partial nephrectomy was 99.2% for Whites and 93.8% for Blacks (19,20), suggesting RCC tissue is relatively mature differentiation and the potential for lower HMGA1 expression within the tumor and higher expression in the adjacent normal tissues; (III) concerning HMGA1 protein expression, it’s pivotal to recognize that proteins serve as the primary functional entities in cellular processes. In the context of ccRCC, it remains uncertain whether HMGA1 mRNA undergoes complete translation to produce corresponding proteins, and if these translated proteins exhibit stability without undergoing degradation pathways, such as ubiquitination. In summary, delineating the expression and function of HMGA1 in ccRCC requires integration with relevant research results and targeted cellular assays.

Due to the addition of new references, the references list and in-text citations should be renumbered. The updated reference should be updated as follows:

1. Sumter TF, Xian L, Huso T, et al. The High Mobility Group A1 (HMGA1) Transcriptome in Cancer and Development. Curr Mol Med 2016;16:353-93.

2. Wang Y, Hu L, Zheng Y, et al. HMGA1 in cancer: Cancer classification by location. J Cell Mol Med 2019;23:2293-302.

3. Frasca F, Rustighi A, Malaguarnera R, et al. HMGA1 inhibits the function of p53 family members in thyroid cancer cells. Cancer Res 2006;66:2980-9.

4. Zhong J, Liu C, Zhang QH, et al. TGF-beta1 induces HMGA1 expression: The role of HMGA1 in thyroid cancer proliferation and invasion. Int J Oncol 2017;50:1567-78.

5. Xian L, Georgess D, Huso T, et al. HMGA1 amplifies Wnt signalling and expands the intestinal stem cell compartment and Paneth cell niche. Nat Commun 2017;8:15008.

6. Resar L, Chia L, Xian L. Lessons from the Crypt: HMGA1-Amping up Wnt for Stem Cells and Tumor Progression. Cancer Res 2018;78:1890-7.

7. Liang L, Li X, Zhang X, et al. MicroRNA-137, an HMGA1 target, suppresses colorectal cancer cell invasion and metastasis in mice by directly targeting FMNL2. Gastroenterology 2013;144:624-35.e4.

8. Chandrasekaran KS, Sathyanarayanan A, Karunagaran D. MicroRNA-214 suppresses growth, migration and invasion through a novel target, high mobility group AT-hook 1, in human cervical and colorectal cancer cells. Br J Cancer 2016;115:741-51.

9. Chiefari E, Foti DP, Sgarra R, et al. Transcriptional Regulation of Glucose Metabolism: The Emerging Role of the HMGA1 Chromatin Factor. Front Endocrinol (Lausanne) 2018;9:357.

10. Williams MD, Xian L, Huso T, et al. Fecal Metabolome in Hmga1 Transgenic Mice with Polyposis: Evidence for Potential Screen for Early Detection of Precursor Lesions in Colorectal Cancer. J Proteome Res 2016;15:4176-87.

11. Williams MD, Zhang X, Belton AS, et al. HMGA1 drives metabolic reprogramming of intestinal epithelium during hyperproliferation, polyposis, and colorectal carcinogenesis. J Proteome Res 2015;14:1420-31.

12. Panneerselvam J, Srivastava A, Muralidharan R, et al. IL-24 modulates the high mobility group (HMG) A1/miR222 /AKT signaling in lung cancer cells. Oncotarget 2016;7:70247-63.

13. Zou H, Ye H, Kamaraj R, et al. A review on pharmacological activities and synergistic effect of quercetin with small molecule agents. Phytomedicine 2021;92:153736.

14. Liu Z, Wang R, Zhu G. Circ_0035483 Functions as a Tumor Promoter in Renal Cell Carcinoma via the miR-31-5p-Mediated HMGA1 Upregulation. Cancer Manag Res 2021;13:693-706.

15. Takaha N, Sowa Y, Takeuchi I, et al. Expression and role of HMGA1 in renal cell carcinoma. J Urol 2012;187:2215-22.

16. Zhang W, Lu Y, Shi H, et al. LncRNA ITGB2-AS1 promotes the progression of clear cell renal cell carcinoma by modulating miR-328-5p/HMGA1 axis. Hum Cell 2021;34:1545-57.

17. Chi XG, Meng XX, Ding DL, et al. HMGA1-mediated miR-671-5p targets APC to promote metastasis of clear cell renal cell carcinoma through Wnt signaling. Neoplasma 2020;67:46-53.

18. Hoadley KA, Yau C, Hinoue T, et al. Cell-of-Origin Patterns Dominate the Molecular Classification of 10,000 Tumors from 33 Types of Cancer. Cell 2018;173:291-304 e6.

19. Siegel RL, Miller KD, Wagle NS, et al. Cancer statistics, 2023. CA Cancer J Clin 2023;73:17-48.

20. Chow WH, Shuch B, Linehan WM, et al. Racial disparity in renal cell carcinoma patient survival according to demographic and clinical characteristics. Cancer 2013;119:388-94.

21. Huang R, Huang D, Dai W, et al. Overexpression of HMGA1 correlates with the malignant status and prognosis of breast cancer. Mol Cell Biochem 2015;404:251-7.

22. Cao XP, Cao Y, Zhao H, et al. HMGA1 promoting gastric cancer oncogenic and glycolytic phenotypes by regulating c-myc expression. Biochem Biophys Res Commun 2019;516:457-65.

23. Cheng Y, Cheng T, Zhao Y, et al. HMGA1 exacerbates tumor progression by activating miR-222 through PI3K/Akt/MMP-9 signaling pathway in uveal melanoma. Cell Signal 2019;63:109386.

24. Wang YT, Pan SH, Tsai CF, et al. Phosphoproteomics Reveals HMGA1, a CK2 Substrate, as a Drug-Resistant Target in Non-Small Cell Lung Cancer. Sci Rep 2017;7:44021.

25. D'Angelo D, Mussnich P, Rosa R, et al. High mobility group A1 protein expression reduces the sensitivity of colon and thyroid cancer cells to antineoplastic drugs. BMC Cancer 2014;14:851.

The authors sincerely apologize for the error and state that this does not affect the scientific conclusions of the article.

Click here to view the updated version of the article.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.


References

  1. E. MP. High-mobility group A1 (HMGA1) gene expressions in various colorectal cancer cell lines and correlation with prognosis. Transl Cancer Res 2020;9:763-73. [Crossref] [PubMed]
Cite this article as: Editorial Office. Erratum to hypofractionation in prostate cancer radiotherapy. Transl Cancer Res 2024;13(1):480-483. doi: 10.21037/tcr-2023-09

Download Citation