Prognostic value of MACC1 and proficient mismatch repair status for recurrence risk prediction in stage II colon cancer patients: the BIOGRID studies

Rohr, Ulrich-Peter; Herrmann, Pia; Ilm, Katharina; Hai, Zhang; Lohmann, Sabine; Reiser, Astrid; Murányi, Andrea; Smith, Janice; Burock, Susen; Osterland, Marc; Leith, Katherine; Singh, Shalini; Brunhoeber, Patrick; Bowermaster, Rebecca; Tie, Jeanne; Christie, Michael; Wong, Hui‐Li; Waring, Paul; Shanmugam, Kandavel; Gibbs, Peter; Stein, Ulrike

doi:10.1093/annonc/mdx207

Cited by 25 publications

(21 citation statements)

References 22 publications

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“…Our study proves that MACC1 is elevated in patients with lung adenocarcinoma and that MACC1 knockdown significantly attenuates proliferation capability, induces G0/ G1 phase arrest and stimulates cell apoptosis in vitro in lung adenocarcinoma cells by regulating the β-catenin pathway. MACC1 elevated expression and prognostic value have been demonstrated in multiple tumors [6,10,[14][15][16][17][18], and our results of tissue samples and database search coincide with the well-documented NSCLC data provided by Wang et al and Zhou et al [10,11]. Numerous studies on the correlation between MACC1 expression and clinical pathological parameters indicate its prognostic value in a variety of cancers [5,8,19].…”

Section: Macc1 Knockdown Effects On Cell Proliferation Cell Cycle Ansupporting

confidence: 87%

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

Guo

et al. 2018

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It has been documented that over-expression of metastasis-associated in colon cancer-1 (MACC1) is related to poor prognosis in non-small cell lung cancer (NSCLC). This study investigates the function and underlying molecular mechanisms of MACC1 in lung adenocarcinoma. Here, we firstly employed immunohistochemistry, western blotting, real-time PCR, and online database to demonstrate that MACC1 expression was elevated in tumor tissues compared with tumoradjacent or normal tissues. Real-time PCR, CCK-8, colony formation western blotting, Hoechst staining, and flow cytometry assays then evaluated the effects of MACC1 knockdown on the cell cycle, cell proliferation and apoptosis in A549 and H1299 adenocarcinoma cells. Result highlighted that MACC1 knockdown inhibited cell proliferation, induced G0/ G1 phase arrest and promoted cell apoptosis in vitro. Mechanistic analysis revealed it also up-regulated expression levels of bax, cleaved-caspase-3 and cleaved-PARP while down-regulating cyclin D1, c-myc, bcl-2, and β-catenin expression in A549 cells. Intriguingly, up-regulation of β-catenin suppressed G0/G1 phase arrest and apoptosis in MACC1-silenced A549 cells and this was accompanied by increased levels of cyclin D1, c-myc, and bcl-2. Collectively, our results indicate that MACC1 knockdown effectively inhibited cell proliferation and promoted apoptosis of lung adenocarcinoma cells by regulating the β-catenin pathway.

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Section: Macc1 Knockdown Effects On Cell Proliferation Cell Cycle Ansupporting

confidence: 87%

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

Guo

et al. 2018

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“…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]. MACC1 is a transcription factor that up-regulates c-Met expression, thereby activating HGF/c-Met signaling pathway and promoting tumor proliferation, invasion, metastasis and survival [11]. It is reported that MACC1 is up-regulated in NPC and promotes tumor invasion and metastasis [12].…”

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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“…Sample sizes of the selected studies ranged from 32 to 2693 (median, 266). Among these studies, 21 studies were conducted in Europe, 12 studies in Asia, 6 studies in America, 3 studies in Australia, and the remaining 9 studies were multicenter studies . Twenty‐seven studies were specifically restricted to patients with colon cancer, while other 24 studies investigated patients with colorectal cancer.…”

Section: Resultsmentioning

confidence: 99%

“…Sample sizes of the selected studies ranged from 32 to 2693 (median, 266). Among these studies, 21 studies were conducted in Europe, 6,17,[30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][48] 12 studies in Asia, [49][50][51][52][53][54][55][56][57][58][59][60] 6 studies in America, 16,[61][62][63][64][65] 3 studies in Australia, [66][67][68] and the remaining 9 studies were multicenter studies. [69][70][71][72][73][74][75][76]…”

Section: Study Characteristicsmentioning

confidence: 99%

Prognostic and predictive role of DNA mismatch repair status in stage II‐III colorectal cancer: A systematic review and meta‐analysis

et al. 2019

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DNA mismatch repair (MMR) status was considered to be a potential prognostic factor for colorectal cancer (CRC) but with conflicting reports, and varied in terms of TNM stages. Its relationship with prognosis in stage II-III CRC had not yet been systematically established. Therefore, we retrieved eligible studies published through May 2019, and screened out 51 studies that reported survival data (overall survival [OS] and/or disease-free survival [DFS]) in 28 331 CRC patients at stage II-III, totally 16.4% of whom were characterized as deficient MMR (dMMR). Significant associations of dMMR status were observed with longer OS (Hazard Ratio [HR] = 0.74, 95% CI: 0.68-0.82; P < .001), as well as DFS (HR = 0.67, 95% CI: 0.59-0.75, P < .001). However, dMMR patients received no statistically significant benefit from fluoropyrimidine-based treatment for either OS (HR = 0.84, 95%CI: 0.60-1.17; P = .31) or DFS (HR = 0.83, 95%CI: 0.60-1.15; P = .27), compared with that in proficient MMR (pMMR) patients for both OS (HR = 0.55, 95% CI: 0.43-0.71; P < .001)and DFS (HR = 0.60, 95% CI: 0.50-0.73; P < .001). Our analysis indicate that dMMR CRC patients at stage II-III had higher OS and DFS than pMMR ones, and fluoropyrimidine-based chemotherapy could improve survival in pMMR patients rather than dMMR ones.chemotherapy, colorectal cancer, DNA mismatch repair, prognosis † Zhujun Deng and Yun Qin contributed equally to this work

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Prognostic value of MACC1 and proficient mismatch repair status for recurrence risk prediction in stage II colon cancer patients: the BIOGRID studies

Abstract: MACC1 expression stratifies colon cancer patients with unfavorable pMMR status. Stage II colon cancer patients with pMMR/MACC1-low tumors have a similar favorable prognosis to those with dMMR with potential implications for the role of adjuvant therapy.

Cited by 25 publications

References 22 publications

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

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

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

Prognostic and predictive role of DNA mismatch repair status in stage II‐III colorectal cancer: A systematic review and meta‐analysis

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