MACC1 silencing inhibits cell proliferation and induces cell apoptosis of lung adenocarcinoma cells through the β-catenin pathway

Guo, Li; Ou, Songlei; Ma, Xinrong; Zhang, S; Lai, Yongqiang

doi:10.4149/neo_2018_170918n595

Cited by 16 publications

(12 citation statements)

References 33 publications

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“…Scholars reported MACC acted as an oncogene involved in cancer progress and metastasis and predicted a poor prognosis in many cancers (17)(18)(19)(20)(21)(22)(23)(24)(25). Moreover, many scholars revealed that MACC1 expression has also been associated with treatment response via interrupting Notch pathway (26), b-catenin (27,28), and HGF/cMet pathway (29). These investigations implicate MACC1 as a multifunctional regulator of cancer progression.…”

Section: Introductionmentioning

confidence: 99%

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

Lei

Chen

et al. 2021

Front. Oncol.

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BackgroundLncRNA-FGD5-AS1, as an oncogene, participates in the development and progress of various cancers. However, the exact role and the molecular mechanisms by which FGD5-AS1 regulates radiosensitivity in breast cancer (BC) remains largely unknown.MethodsWe used X-Ray weekly-dose-increase method to establish radiation-resistance cell lines. Bioinformatics tools analyze the expression of FGD5-AS1 in breast cancer tissue and evaluated the relationship between FGD5-AS1 and clinic-pathological features. CCK-8 and colony formation were used to analyze cell proliferation. Western blotting and qPCR were applied to detect protein and gene expression, respectively. RNA interference was used to knock down the endogenous gene expression. Luciferase reporter system and immunoprecipitates were applied to verify the target of FGD5-AS1.ResultFGD5-AS1 was overexpressed in BC tissues and radiation-resistance cell lines. Higher levels of FGD5-AS1 predicted poorer clinical characteristics and prognosis. Loss-of-function FGD5-AS1 sensitized BC cells to X-ray, meanwhile, the cell gained radiation-resistance when exogenous FGD5-AS1 was expressed. FGD5-AS1 depletion arrested cells at G0/G1 and triggers cell apoptosis. The starBase database (ENCORI), predicted binding site of miR-497-5p in FGD5-AS1 sequence, and luciferase reporter system and immunoprecipitates verified miR-497-5p was the target of FGD5-AS1. Furthermore, MACC1 was predicted and verified as the target of miR-497-5p. Loss-of-function FGD5-AS1 sensitized ionizing radiation was rescued by the up-regulation of MACC1 and the inhibition of miR-497.ConclusionFGD5-AS1 displays an oncogene profile in CRC; patients with high expression of FGD5-AS1 should benefit less from radiotherapy and need a more frequent follow-up. Besides, FGD5-AS1 may be a potential therapeutic target for CRC.

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Section: Introductionmentioning

confidence: 99%

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

Lei

Chen

et al. 2021

Front. Oncol.

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“…For example, MACC1 improves the cisplatin resistance partially in lung cancer via the PI3K/AKT pathway, 51 whereas its depletion suppresses lung cancer cell proliferation and causes cell apoptosis through the β-catenin pathway. 52 Furthermore, MACC1 is implicated in the control of HGF/Met and MEK/ERK pathways in ovarian cancer, 53 Akt/β-catenin pathway in nasopharyngeal carcinoma, 54 and HGF/c-MET/AKT pathway in hepatocellular carcinoma. 55 Our study did not explore the effects of LINC00519 on these signaling pathways that were under the control of MACC1.…”

Section: Discussionmentioning

confidence: 99%

<p>Long Intergenic Non-Protein Coding RNA 519 Promotes the Biological Activities of Tongue Squamous Cell Carcinoma by Sponging microRNA-876-3p and Consequently Upregulating MACC1</p>

Liu

Zhao

Wang

et al. 2020

OTT

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Long intergenic non-protein coding RNA 519 (LINC00519) promotes the development of lung squamous cell carcinoma. In this study, we detected the expression of LINC00519 in tongue squamous cell carcinoma (TSCC) and examined its clinical significance. Additionally, the regulatory effects of LINC00519 on behaviors of TSCC tumor cells were explored through functional experiments. Finally, mechanistic studies were performed to elucidate the molecular events underlying the tumor-promoting actions of LINC00519 in TSCC. Materials and Methods: The expression of LINC00519 in TSCC tissues and cell lines was determined using quantitative reverse transcription-polymerase chain reaction. Cell counting kit-8 assay, flow cytometric analysis, cell migration and invasion assays and xenograft tumor model analyses were used to detect TSCC cell proliferation, apoptosis, migration and invasion and in vivo tumor growth, respectively. Mechanistic studies were performed using bioinformatics analysis, RNA immunoprecipitation assay, luciferase reporter assay and rescue experiments. Results: LINC00519 was overexpressed in both TSCC tissues and cell lines. A high LINC00519 level was associated with poor overall survival in patients with TSCC. In vitro, LINC00519 played cancer-promoting roles in TSCC progression by facilitating cell proliferation, migration and invasion and restraining cell apoptosis. In vivo, LINC00519 downregulation resulted in decreased TSCC tumor growth. Mechanistically, LINC00519 acted as a competing endogenous RNA for microRNA-876-3p (miR-876-3p), which directly targets metastasis associated with colon cancer-1 (MACC1), in TSCC cells. LINC00519 upregulated the expression of MACC1 in TSCC cells by sequestering miR-876-3p. Rescue experiments further affirmed that miR-876-3p inhibition or MACC1 overexpression mitigated the inhibitory influences of LINC00519 depletion on cell proliferation, migration and invasion and neutralized the promoting actions of LINC00519 knockdown on cell apoptosis in TSCC. Conclusion: LINC00519 aggravated the oncogenicity of TSCC by regulating the miR-876-3p/MACC1 axis. Our findings suggest that the LINC00519/miR-876-3p/MACC1 pathway may be an underlying therapeutic target in TSCC.

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“…Cell cycle analysis. The cell cycle distribution was detected using a propidium iodide (PI)-based cell cycle analysis kit (Beyotime Institute of Biotechnology), as previously described (20). The principle of this method is that the nuclei of dead cells can be stained by PI.…”

Section: Methodsmentioning

confidence: 99%

Downregulation of ENDOCAN in myeloid leukemia cells inhibits proliferation and promotes apoptosis by suppressing nuclear factor‑κB activity

Sun

et al. 2019

Mol Med Report

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Previous studies have demonstrated that ENDOCAN is elevated in leukemia, and it has been reported to be associated with poor prognosis. However, the functional role of ENDOCAN in the development of leukemia remains to be fully elucidated. In the present study, the expression levels of ENDOCAN were detected in THP-1, U937, HL-60 and K562 cells, and it was found that ENDOCAN was increased in U937 and K562 cells, compared with the other two cell lines. Subsequently, ENDOCAN was knocked down in U937 and K562 cells via lentiviral infection. It was found that cell proliferation and the expression of proliferating cell nuclear antigen were inhibited in myeloid leukemia cells following the silencing of ENDOCAN. ENDOCAN knockdown induced G0/G1-phase cell cycle arrest in myeloid leukemia cells with a decreased expression of cyclin D1. Furthermore, cell apoptosis was increased in response to ENDOCAN silencing, which was accompanied by the downregulation of B-cell lymphoma (BCL2) and the upregulation of BCL2-associated X protein, cleaved caspases 3 and 9, and cleaved poly (ADP-ribose) polymerase. Furthermore, it was demonstrated that the knockdown of ENDOCAN inhibited nuclear factor-κB (NF-κB) activity, as evidenced by the increased expression of NF-κB inhibitor α (IκBα), decreased expression of phosphorylated (p-)IκBα, p-P65 and nuclear P65, and reduced NF-κB DNA-binding activity. In combination, the present findings suggested that ENDOCAN may serve as a potential therapeutic target in the treatment of leukemia.

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MACC1 silencing inhibits cell proliferation and induces cell apoptosis of lung adenocarcinoma cells through the β-catenin pathway

Cited by 16 publications

References 33 publications

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

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

<p>Long Intergenic Non-Protein Coding RNA 519 Promotes the Biological Activities of Tongue Squamous Cell Carcinoma by Sponging microRNA-876-3p and Consequently Upregulating MACC1</p>

Downregulation of ENDOCAN in myeloid leukemia cells inhibits proliferation and promotes apoptosis by suppressing nuclear factor‑κB activity

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