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. 2022 Mar 29;12:799475. doi: 10.3389/fonc.2022.799475

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Copyright © 2022 Zhu, Huang, Peng, Luo, Liu, Liu, Wu and Luo

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Unfavorable impact of AC108134.2 on PAAD in vitro. (A) qRT-PCR analysis of AC108134.2 mRNA levels in PAAD tissues and corresponding adjacent tissues (n = 29). (B) The knockdown efficiency of AC108134.2 expression in BxPC-3 cells was verified through qRT-PCR. (C) CCK-8 assay was used to detect the changes in cell viability of BxPC-3 cells following silencing of AC108134.2. (D) Wound healing array was used to analyze the wound healing of BxPC-3 cells downregulated by AC108134.2. (E) Changes in the proliferation rate of BxPC-3 cells after silencing of AC108134.2 were analyzed through EdU staining. (F) Transwell invasion assay was used to analyze changes in the invasive ability of BxPC-3 cells after silencing of AC108134.2 (G) Western blot analysis of the expression of genomic instability-related proteins (MLH1, MSH2, and MSH6) after knockdown of AC108134.2. The CPTAC tool was used to analyze the protein expression levels of MLH1 (H), MSH2 (J), and MSH6 (L) in PAAD. GEPIA2.0 server was used to analyze the overall survival rate of MLH1 (I), MSH2 (K), MSH6 (M) high, and low expression groups in PAAD.*p < 0.05, **p < 0.01, ***p < 0.001. ns stands for p > 0.05.