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RETRACTED ARTICLE: Silencing POLE2 promotes apoptosis and inhibits proliferation of oral squamous cell carcinomas by inhibiting PI3K/AKT signaling pathway

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This article was retracted on 26 April 2024

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Abstract

Oral squamous cell carcinoma is the most common malignant tumor in the head and neck at present, but the mechanism of its occurrence and development is still unclear, and there is still a lack of effective targeting drugs. The second major subunit of DNA polymerase (POLE2) has exonuclease activity and can catalyze the replication and modification of new chains. Our previous studies have found that it is associated with OSCC progression, but the mechanism is unclear.The expression of POLE2 in OSCC was detected by immunological method. The expression of POLE2 was inhibited in OSCC cells, and the biological function of the cells was detected by RT-PCR and Western Blot. Cell proliferation, apoptosis and migration were detected by colony formation, MTT, flow cytometry, wound healing and Transwell. The expression level of POLE2 gene in OSCC was significantly higher than that in normal tissues. In addition, the expression level of POLE2 gene was significantly different from the tumor type and prognosis. During the development of oral squamous cell carcinoma, silencing POLE2 inhibits the proliferation of oral cancer cells and promotes apoptosis. The results of animal experiments also support the positive correlation between POLE2 and OSCC progression. We further demonstrated that POLE2 can up-regulate the downregulation of apoptosis-related proteins such as Caspase3, CD40, CD40L, DR6, Fas, IGFBP-6, P21, and SMAC. In addition, POLE2 regulates OSCC progression by inhibiting the PI3K/AKT pathway. POLE2 is closely related to the progression of OSCC, and POLE2 may be a potential target for OSCC treatment.

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Funding

Funed by National Natural Science Foundation of China “Study on the mechanism of EFNA3 induced oral squamous cell carcinoma regulated by KMT2D through H3K4me1/H3K27ac” (82203418).

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SG: Contributed to design, acquisition, analysis, and interpretation, drafted manuscript, critically revised manuscript. KW: Contributed to design, acquisition, and interpretation, drafted manuscript, critically revised manuscript, gave final approval and agree to be accountable for all aspects of work ensuring integrity and accuracy. YM: Contributed to analysis, and interpretation, drafted manuscript, critically revised manuscript, gave final approval and agree to be accountable for all aspects of work ensuring integrity and accuracy. ZH: Contributed to design, acquisition, and interpretation,drafted manuscript, critically revised manuscript, gave final approval and agree to be accountable for all aspects of work ensuring integrity and accuracy. XY: Contributed to analysis, and interpretation, drafted manuscript, critically revised manuscript, gave final approval and agree to be accountable for all aspects of work ensuring integrity and accuracy. WS: Contributed to design, acquisition, and interpretation, drafted manuscript, critically revised manuscript, gave final approval and agree to be accountable for all aspects of work ensuring integrity and accuracy. LW: Contributed to design, acquisition, and interpretation, drafted manuscript, critically revised manuscript, gave final approval and agree to be accountable for all aspects of work ensuring integrity and accuracy. All authors gave their final approval and agree to be accountable for all aspects of the work.

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Correspondence to Wei Shang or Lin Wang.

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All authors have no direct conflict of interest.

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Informed consent was obtained from each patient for this retrospective study.

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This article has been retracted. Please see the retraction notice for more detail:https://doi.org/10.1007/s12032-024-02377-7

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Ge, S., Wang, K., Meng, Y. et al. RETRACTED ARTICLE: Silencing POLE2 promotes apoptosis and inhibits proliferation of oral squamous cell carcinomas by inhibiting PI3K/AKT signaling pathway. Med Oncol 40, 304 (2023). https://doi.org/10.1007/s12032-023-02158-8

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  • DOI: https://doi.org/10.1007/s12032-023-02158-8

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