A pan-cancer analysis of the prognostic and immunological role of β-actin (ACTB) in human cancers

Abstract

Beta-actin (ACTB), a highly conserved cytoskeleton structural protein, has been regarded as a common housekeep gene and used as a reference gene for years. However, accumulating evidence indicates that ACTB is abnormally expressed in multiple cancers and hence changes the cytoskeleton to affect the invasiveness and metastasis of tumors. This study aimed to investigate the function and clinical significance of ACTB in pan-cancer. The role of ACTB for prognosis and immune regulation across 33 tumors was explored based on the datasets of gene expression omnibus and the cancer genome atlas. Differential expression of ACTB was found between cancer and adjacent normal tissues, and significant associations was found between ACTB expression and prognosis of tumor patients. In most cancers, ACTB expression was associated with immune cells infiltration, immune checkpoints and other immune modulators. Relevance between ACTB and metastasis and invasion was identified in various types of cancers by CancerSEA. Moreover, focal adhesion and actin regulation-associated pathways were included in the functional mechanisms of ACTB. The expression of ACTB was verified by quantitative real-time polymerase chain reaction. Knockdown of ACTB inhibited head and neck squamous carcinoma cell migration and invasion by NF-κB and Wnt/β-catenin pathways. Our first pan-cancer study of ACTB offers insight into the prognostic and immunological roles of ACTB across different tumors, indicating ACTB may be a potential biomarker for poor prognosis and immune infiltration in cancers, and the role of ACTB as a reference gene in cancers was challenged.

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“…7) indicates that four of them are found associated with breast cancer, including ACTB, TMSB10, PABPC1 and ACTG1 . Study finds differential ACTB expression in breast cancer is associated with metastasis and drug resistance in breast cancer [30]. TMSB10 was upregulated in breast cancer tissues and its overexpression promotes invasion, proliferation and migration of breast cancer cells [31].…”

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“…However, the emerging evidence suggests that ACTB expresses unstably and plays a key role in a variety of human diseases, particularly cancer [ 37 ]. Previous studies showed that the mRNA level of ACTB was down-regulated in esophageal cancer, colon cancer, and LUSC compared to normal tissues [ 38 , 39 ]. The same is also true for ITGB1 .…”

“…However, some other studies found the opposite results, suggesting that ACTB was up-regulated in some cancers, such as esophageal cancer (ES) and NSCLC (not typed) compared to normal samples [ 42 , 43 ], and a study showed that up-regulated ACTB was associated with poor prognosis in LUAD [ 39 ]. These studies did not distinguish between LUAD and LUSC.…”

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“…Three of six 5’- ACTB HFGs resulted in no protein alterations, while the remaining three altered N-termini; ACTB-KLF2 had an ORF without a start codon (Fig.S1). Five 3’- ACTB HFGs encoded intact β-actin; PTMA-ACTB,ELMO1-ACTB, KLF2-ACTB, TPM4-ACTB , and LFNG - ACTB encoded β-actin-involved hybrid proteins; TNRC18-ACTB and OAZ1-ACTB coded for truncated β-actin (Fig.S2), which explained why ACTB , a housekeeping gene, was abnormally expressed in cancer 27 . DDX5-CHD2, DDX5-EEF1A1, DDX5-HNRNPH3 , and DDX5-UBB encoded intact proteins, while DDX5-ATP6V0C , DDX5 -GNAS, DDX5-HNRNPU , and DDX5-SF1 produced truncated proteins (Fig.S3), which were from 43 to 702 aa shorter than their parental counterparts.…”