Downregulation of MACC1 inhibits the viability, invasion and migration and induces apoptosis in esophageal carcinoma cells through the phosphatase and tensin homolog/phosphoinositide 3-kinase/protein kinase B signaling pathway

Qian, Liqiang; Xia-qin, LI; Ye, Peng‑Hui; Su, Haoyuan; Wang, Gang; Liu, Yan; Shen, Genhai; Gao, Quangen

doi:10.3892/ol.2017.6790

Cited by 13 publications

(12 citation statements)

References 30 publications

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“…Down-regulation of RPN2 expression also inhibited tumor growth in vivo , and dramatically reduced tumor size and weight in a xeno-transplanted tumor model. Immoderate migration and invasion of tumor cells are considered crucial in the process of esophageal carcinoma metastasis [20,21]. Cell migration and invasion capabilities of esophageal cancer cells transfected with siRPN2 were then evaluated.…”

Section: Discussionmentioning

confidence: 99%

Ribophorin II promotes cell proliferation, migration, and invasion in esophageal cancer cells in vitro and in vivo

Huang

Bai

et al. 2019

Bioscience Reports

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Esophageal cancer is a common digestive tract cancer, which is a serious threat to human health. Ribophorin II (RPN2) is a part of an N-oligosaccharyltransferase complex, which is excessively expressed in many kinds of cancers. In the present study, we explore the biological role of RNP2 in esophageal cancer. First, we found that the expression of RPN2 was higher in esophageal cancer tissues than in adjacent non-tumor tissues, and negatively correlated with E-cadherin expression. RPN2 expression levels in esophageal cancer tissues were positively associated with differentiation and tumor node metastasis (TNM) stage. Furthermore, the expression of RPN2 was increased significantly in esophageal cancer cell lines compared with normal cells. The effect of RPN2 down-regulation on cell proliferation, cell migration, and cell invasion was examined by cell counting kit-8 (CCK8), wound healing assay, and Transwell assay, respectively. Silencing RPN2 effectively inhibited cell proliferation of esophageal cancer cells in vitro and in vivo. Cell migration and invasion were also weakened dramatically by siRPN2 treatment of esophageal cancer cells. In addition, protein expression of proliferating cell nuclear antigen (PCNA), matrix metalloproteinase (MMP-2), and E-cadherin in esophageal cancer cells was determined by Western blot analysis. PCNA, MMP-2, E-cadherin, Snail and phosphorylation-Smad2/3 expression was also regulated notably by siRPN2 treatment. These findings indicate that RPN2 exhibits oncogenetic capabilities in esophageal cancer, which could provide novel insights into esophageal cancer prevention and treatment.

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Section: Discussionmentioning

confidence: 99%

Ribophorin II promotes cell proliferation, migration, and invasion in esophageal cancer cells in vitro and in vivo

Huang

Bai

et al. 2019

Bioscience Reports

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“…Metastasis-associated in colon cancer-1 (MACC1) is a gene discovered after genomic analysis of human colon cancer tissue, metastatic tumor tissue and human normal tissue [6,7]. Further studies show that the MACC1 gene is highly expressed in a variety of tumors such as colon cancer, liver cancer, and esophageal cancer [8,9]. The protein encoded by MACC1 consists of four domains (ZU5, SH3 and 2 death domains at the hydroxyl terminus), which are closely related to cell signal transduction and apoptosis [10].…”

Section: Introductionmentioning

confidence: 99%

MACC1 facilitates the escape of nasopharyngeal carcinoma cells from killing by natural killer cells

Zhao

Liu

Zeng

et al. 2019

Biotechnology & Biotechnological Equipment

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This study examined the regulation of phenotype and function of natural killer (NK) cells by nasopharyngeal carcinoma (NPC) cells with metastasis-associated in colon cancer-1 (MACC1) overexpression. Thirty patients with NPC and 20 healthy subjects were included. Peripheral blood (5 mL) was collected, and NK cells were purified using Ficoll and negative separation. NPC HONE1 cells were transfected with pcDNA3.1-MACC1 or negative control plasmids, and culture supernatant was collected for co-culture with NK cells. Flow cytometry was used to determine the expression of activated and inhibitory receptors on the cells. Western blotting was used to determine the expression of proteins. The results showed that the ratio of NK cells in the peripheral blood of NPC patients was elevated, but the activity and tumor-killing effect of NK cells were reduced. MACC1 promoted the escape of HONE1 cells from killing by NK cells. HONE1 with overexpression of MACC1 down-regulated the expression of NKG2D in NK cells, inhibited the proliferation of NK cells and escaped the immune surveillance by NK cells. MACC1 downregulated the expression of NKG2D in NK cells by up-regulating the expression of TGF-b1 in HONE1 cells, thereby inhibiting the activity of NK cells. MACC1 inhibited the cell cycle of NK cells via TGF-b1 pathway. The study demonstrated that MACC1 elevated the expression of TGF-b1 by NPC HONE1 cells, thereby inhibiting NKG2D expression and G1/S transition in NK cells. MACC1 helped NPC HONE1 cells avoid killing by NK cells.

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“…MACC1, which is located on human chromosome 7 (7p21.1), 49 is upregulated in TSCC and is closely associated with lymphatic metastasis. 50 In TSCC patients, increased MACC1 expression tends to be associated with worse clinical outcomes. 50 MACC1 is considered the main regulator of tumor progression in TSCC, in which it affects a number of malignant processes.…”

Section: Discussionmentioning

confidence: 99%

“…50 In TSCC patients, increased MACC1 expression tends to be associated with worse clinical outcomes. 50 MACC1 is considered the main regulator of tumor progression in TSCC, in which it affects a number of malignant processes. 33,50 MACC1 affected cancer progression through different mechanisms.…”

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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Downregulation of MACC1 inhibits the viability, invasion and migration and induces apoptosis in esophageal carcinoma cells through the phosphatase and tensin homolog/phosphoinositide 3-kinase/protein kinase B signaling pathway

Cited by 13 publications

References 30 publications

Ribophorin II promotes cell proliferation, migration, and invasion in esophageal cancer cells in vitro and in vivo

Ribophorin II promotes cell proliferation, migration, and invasion in esophageal cancer cells in vitro and in vivo

MACC1 facilitates the escape of nasopharyngeal carcinoma cells from killing by natural killer cells

<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>

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