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American Journal of Cancer Research logoLink to American Journal of Cancer Research
. 2025 Oct 25;15(10):4604–4607. doi: 10.62347/SLDR4832

MicroRNA-625 inhibits the proliferation and increases the chemosensitivity of glioma by directly targeting AKT2

Jiale Zhang 1,*, Jian Zhang 1,*, Jie Zhang 1,*, Wenjin Qiu 2, Shuo Xu 1, Qun Yu 1, Chengke Liu 3, Yingyi Wang 1, Ailin Lu 1, Junxia Zhang 1, Xiaoming Lu 1
PMCID: PMC12616173  PMID: 41244124

We recently discovered that the ‘GAPDH’ panel in Figure 5C and the ‘CDK4’ panel in Figure 5I are very similar. Similarly, parts of the data in Figures 2B and 5B also show similarities, while the data in Figures 4F and 5F closely match those from our team’s previous articles. The authors re-examined the data and found that the selection of data panels in these charts was incorrect, which is an editorial error. With the agreement of all authors, we have revised Figures 4F, 5B, 5C and 5F. Therefore, we would like to publish this Erratum to reflect this change. We apologize for any confusion it may have caused. The corrections made in this erratum do not affect the final conclusions. The corrected Figures 4 and 5 are as follows.

Figure 5.

Figure 5

AKT2 reverses the inhibitory effects of miR-625 on cell proliferation in vitro. A. Western blot analysis of AKT2 expression in U87 and U251 cells after AKT2 overexpression. GAPDH served as the loading control. B. Colony formation assay performed in AKT2-overexpressing U87 and U251 cells. **P<0.01. C. Western blot analysis showing reduced AKT2 expression in cells after AKT2 knockdown. GAPDH served as the loading control. D. Representative images of colony formation assays using U87 and U251 cells transiently transfected with siAKT2 and siNC. **P<0.01. E. Cell viability rates were assayed in miR-NC, miR-625 and miR-625+AKT2 co-transfected U87 and U251 cells by the CCK-8 assay. *P<0.05. F. Representative images of colony formation assays using the above cells. **P<0.01. G. Representative images of the EdU assay in the above cells. **P<0.01. H. Cell cycle profiles were examined in miR-NC, miR-625 or miR-625+AKT2 co-transfected U87 and U251 cells by flow cytometry. I. A rescue experiment was performed by introducing pcDNA3.1-AKT2 in the presence of ectopic miR-625 expression in U87 and U251 cells. Western blot analysis of Cyclin D1, Cyclin E1 and CDK6 in the indicated cells. GAPDH was used as the loading control.

Figure 4.

Figure 4

MiR-625 overexpression suppressed tumor growth in vivo. A. Tumor growth curves measured after injecting U87 cells stably expressing miR-NC or miR-625. Tumor volumes were calculated every 3 d from days 3-30. Tumor volumes were measured by a Vernier caliper on the indicated days. **P<0.01; ***P<0.001. B. Representative images of subcutaneous tumors 30 d after inoculation. C. Tumor weights were measured in the miR-NC and miR-625 groups after tumors were harvested. **P<0.01. D. AKT2, Ki-67 and cleaved caspase 3 levels were analyzed in tumor tissues by immunohistochemistry; representative images are shown. Magnification, ×200. E. AKT2 expression in tumors from the miR-625 and miR-NC groups was measured by immunofluorescence. Magnification, ×200. F. Western blot analysis of AKT2 in tumors derived from U87 cells after treatment with miR-625 mimic or vector control. GAPDH was used as the loading control.


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