LncRNA FGD5-AS1 promotes tumor growth by regulating MCL1 via sponging miR-153-3p in oral cancer

Abstract

Purpose: To investigate the function of long noncoding RNA (lncRNA) FGD5-AS1 in oral cancer (OC) and to further clarify the regulation of FGD5-AS1 on miR-153-3p/MCL1 axis. Results: FGD5-AS1 was significantly increased in OC tissues and cells. Loss of FGD5-AS1 inhibited the proliferation, migration and invasion of OC cells. FGD5-AS1 acted as a sponge of miR-153-3p, and MCL1 was direct target of miR-153-3p. Forced expression of miR-153-3p or inhibition of MCL1 reversed the promoted role of FGD5-AS1 on OC cells’ migration and invasion. The in vivo tumor growth assay showed that FGD5-AS1 promoted OC tumorigenesis by regulating miR-153-3p/MCL1 axis. Conclusions: Our research revealed lncRNA FGD5-AS1 acted as an oncogene by regulating MCL1 via sponging miR-153-3p, thus providing some novel experimental basis for clinical treatment or prevention of OC. Patients and Methods: The mRNA expression of FGD5-AS1, miR-153-3p and MCL1 was detected by qRT-PCR. CCK8 assay, Edu assay, wound healing assay and transwell assay were used to detect the FGD5-AS1/ miR-153-3p/MCL1 axis function on proliferation, migration and invasion in OC cells. Western blot was used to calculate protein level of MCL1. Luciferase assay was used to detect the binding of miR-153-3p and MCL1, FGD5-AS1and miR-153-3p.

The LncRNA FGD5‐AS1/miR‐497‐5p axis regulates septin 2 (SEPT2) to accelerate cancer progression and increase cisplatin‐resistance in laryngeal squamous cell carcinoma

“…LncRNA FGD‐AS1 plays a tumor‐promoting role in CRC, 29 oral cancer, 30 and renal cell carcinoma, 31 but no literature reports the involvement of LncRNA FGD‐AS1 in regulating LSCC development. Based on this, the present study reports that knock‐down of LncRNA FGD‐AS1 suppresses LSCC progression, indicating that targeting LncRNA FGD‐AS1 hampers cancer development in LSCC, which are supported by the previous work in other types of cancer 29–31 .…”

“…LncRNA FGD‐AS1 plays a tumor‐promoting role in CRC, 29 oral cancer, 30 and renal cell carcinoma, 31 but no literature reports the involvement of LncRNA FGD‐AS1 in regulating LSCC development. Based on this, the present study reports that knock‐down of LncRNA FGD‐AS1 suppresses LSCC progression, indicating that targeting LncRNA FGD‐AS1 hampers cancer development in LSCC, which are supported by the previous work in other types of cancer 29–31 . In addition, the inhibiting effects of LncRNA FGD‐AS1 ablation on LSCC development are abrogated by knocking down miR‐497‐5p and upregulating SEPT2, implying that the LncRNA FGD‐AS1/miR‐497‐5p/SEPT2 signaling cascade involves in regulating LSCC progression, which is in accordance with the ceRNA mechanisms 23–25 .…”

“…The long noncoding RNAs (LncRNAs)‐microRNAs (miRNAs)‐mRNA competing endogenous RNA (ceRNA) networks are crucial for regulating cancer progression, 23–25 and researchers also report that targeting the ceRNA networks is effective to hamper the development of LSCC 26–28 . Among all the LncRNAs, LncRNA FGD5‐AS1 is identified as an oncogene to promote the development of colorectal cancer (CRC), 29 oral cancer, 30 and renal cell carcinoma 31 . In addition, elevated LncRNA FGD5‐AS1 contributes to cisplatin‐resistance in NSCLC cells 32 and lung adenocarcinoma cells 33 .…”

LncRNA FGD5-AS1 Facilitates the Radioresistance of Breast Cancer Cells by Enhancing MACC1 Expression Through Competitively Sponging miR-497-5p

“…As previously described, lncRNA FGD5-AS1 participated as an essential mediator in various cancer. As we reviewed the published paper, lncRNA FGD5-AS1 might serve as a prognosis factor of colon cancer, oral cancer, and melanoma (38)(39)(40)(41)(42)(43). Scholars araised interest of lncRNA FGD5-AS1 from 2018, and reported different molecular mechanism of lncRNA FGD5-AS1 in various cancer, including: regulating miR-140-5p/WEE1 axis (44), miR-153-3p/CITED2 (40), ERK/AKT signaling (45), MCL1 (42), Wnt/b-catenin (28,46), miR-103a-3p/TPD52 (47).…”

Long Non-Coding RNAs as Functional Codes for Oral Cancer: Translational Potential, Progress and Promises

“…Notably, the cytoplasmic abundant lncRNA, RC3H2, could physically interact with miR-101-3p, while suppression of miR-101-3p could attenuate the lncRNA RC3H2 knockdown-induced inhibitory effects on OSCC cells by targeting EZH2, revealing that lncRNA RC3H2 could act as ceRNA to up-regulate EZH2 expression by sponging miR-101-3p ( Figure 1 d), which subsequently affected the level of H3K27me3 deposition and the expression of downstream genes associated with cancer progression [ 53 , 54 ]. Moreover, the MEG3 [ 55 ], ANRIL [ 56 ], FGD5-AS1 [ 57 ], H19 [ 58 ], HOTAIR [ 37 ], LINC01315 [ 30 ], MALAT1 [ 59 ], PDIA3P [ 60 ], RBM5-AS1 [ 61 ], SNHG20 [ 33 ], TUG1 [ 62 ], and TTN-AS1 [ 63 ] lncRNAs were reported to have the ability to physically interact with miRNAs and thereby influence the development of OSCC. Considering the requirements for appropriate experimental manipulations [ 52 ], such as the well-controlled overexpression of miRNAs within physiological ranges and additional evidence supported by miRNA suppression experiments to avoid the potential saturation of RISC complexes, the claims of ceRNA interactions may require more critical evaluation.…”