AKR1B10 inhibits the proliferation and migration of gastric cancer via regulating epithelial-mesenchymal transition

Shao, Xinyu; Wu, Jue; Yu, Shunying; Zhou, Yuqing; Zhou, Chunli

doi:10.18632/aging.203538

Cited by 15 publications

(18 citation statements)

References 33 publications

(41 reference statements)

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“…To further verify the sequencing results, we performed a PCR array on MSCs and MSC SPIO to analyze the gene expression pattern in the ferroptosis-related signaling pathway. Among genes with significant fold-change, ferroptosis suppresser TF [ 24 , 25 ], and CA9 [ 26 , 27 ], were the most downregulated, and ferroptosis promoter AKR1B10 [ 28 ] was the most upregulated gene (Fig. 3C, D ).…”

Section: Resultsmentioning

confidence: 99%

Ferroptotic MSCs protect mice against sepsis via promoting macrophage efferocytosis

Pan

Wang

et al. 2022

Cell Death Dis

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The therapeutic effect of mesenchymal stem cells (MSCs) on sepsis has been well-known. However, a comprehensive understanding of the relationship between MSCs and macrophages remains elusive. Superparamagnetic iron oxide (SPIO) is one of the most commonly used tracers for MSCs. Our previous study has shown that SPIO enhanced the therapeutic effect of MSCs in a macrophage-dependent manner. However, the fate of SPIO-labeled MSCs (MSCSPIO) after infusion remains unknown and the direct interaction between MSCSPIO and macrophages remains unclear. Mice were injected intravenously with MSCSPIO at 2 h after Escherichia coli infection and sacrificed at different times to investigate their distribution and therapeutic effect. We found that MSCSPIO homed to lungs rapidly after infusion and then trapped in livers for more than 10 days. Only a few MSCSPIO homed to the spleen and there was no MSCSPIO detectable in the brain, heart, kidney, colon, and uterus. MSCSPIO tended to stay longer in injured organs compared with healthy organs and played a long-term protective role in sepsis. The mRNA expression profiles between MSCs and MSCSPIO were rather different, genes related to lipid metabolism, inflammation, and oxidative stress were changed. The levels of ROS and lipid peroxide were elevated in MSCSPIO, which confirmed that SPIO-induced ferroptosis in MSCSPIO. Ferroptosis of MSCSPIO induced by SPIO enhanced the efferocytosis of macrophages and thus enhanced the protective effect on septic mice, while the benefits were impaired after MSCSPIO were treated with Ferrostatin-1 (Fer-1) or Liproxtatin-1 (Lip-1), the inhibitors of ferroptosis. SPIO-induced ferroptosis in MSCs contributes to better therapeutic effects in sepsis by enhancing the efferocytosis of macrophages. Our data showed the efficacy and advantage of MSCSPIO as a therapeutic tool and the cell states exert different curative effects on sepsis.

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Section: Resultsmentioning

confidence: 99%

Ferroptotic MSCs protect mice against sepsis via promoting macrophage efferocytosis

Pan

Wang

et al. 2022

Cell Death Dis

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“…However, the role of AKR1B10 remains unclear. Growing evidence has shown that AKR1B10 is a tumor suppressor [23,24]. Shao et al reported that AKR1B10 expression was significantly related to smaller tumor size, lower depth of invasion, negative lymph node metastasis, negative venous invasion, and advanced tumor stage [23].…”

Section: Discussionmentioning

confidence: 99%

“…Its knockdown could inhibit tumor proliferation and migration by enhancing epithelial-mesenchymal transition (EMT) in vivo. Furthermore, a high expression of AKR1B10 was significantly associated with a better 5-year survival rate [23,24]. In contrast, GC patients with overexpression of AKR1B10 were found to have advanced lymph node metastasis, fewer tumor regression, and worse overall survival (OS) than those without AKR1B10 expression [25].…”

Section: Introductionmentioning

confidence: 99%

Overexpression of AKR1B10 Predicts Poor Prognosis in Gastric Cancer Patients Undergoing Surgical Resection

Liu

Huang

et al. 2022

Current Oncology

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Aldo–keto reductase family 1 member B10 (AKR1B10) is associated with several cancers, but the prognostic role in gastric cancer (GC) remains unclear. We enrolled 359 GC patients who underwent a gastrectomy with D2 lymph node dissection. AKR1B10 expression was scored using an immunoreactive scoring system based on immunohistochemistry. Adjuvant chemotherapy with S-1 or oxaliplatin plus capecitabine was administered to pathological stage II or III disease patients. There were 117 (32.6%) and 242 (67.4%) patients with AKR1B10 overexpression and low expression, respectively. Patients overexpressing AKR1B10 had worse 5-year disease-free survival (DFS) and overall survival (OS) rates than those with low expression of AKR1B10. Pathological T3–T4 stage, pathological stage III, lymph node ratio ≥ 25%, and AKR1B10 overexpression were independent prognostic factors for worse DFS and OS in univariate and multivariate analyses. For 162 stage II or III patients who received adjuvant chemotherapy after surgical resection and 59 patients with signet ring cell carcinoma histology, AKR1B10 overexpression was also associated with inferior DFS and OS. AKR1B10 was not associated with clinical survival in stage I GC patients. In conclusion, AKR1B10 overexpression may be an independent prognostic factor for worse survival in GC patients who underwent gastrectomy with D2 lymph node dissection.

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“…We further predicted that miR-137 was correlated with the expression of Aldo-keto reductase family 1 member B10 (AKR1B10). AKR1B10 possesses potentials in cancer development and progression, which has emerged as a diagnostic target for tumors [ 12 ]. Furthermore, elevated AKR1B10 is detected in steatohepatitis [ 13 ], yet the effect of AKR1B10 on AH deserved explored in-depth.…”

Section: Introductionmentioning

confidence: 99%

LncRNA 1700020I14Rik promotes AKR1B10 expression and activates Erk pathway to induce hepatocyte damage in alcoholic hepatitis

Bai

et al. 2022

Cell Death Discov.

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Alcoholic hepatitis (AH), a kind of alcoholic liver disease, shows poor prognosis. Long noncoding RNAs (lncRNAs) exert critical role in liver diseases. Here, we intended to investigate the possible molecular mechanism that 1700020I14Rik-based regulation of microRNA (miR)-137/Aldo-keto reductase family 1 member B10 (AKR1B10) affecting the inflammatory response and hepatocyte damage in AH. AH-related genes and the down-stream regulatory pathway were screnned by bioinformatics. Mouse normal hepatocyte cell line AML12 was selected to construct an ethanol-induced hepatocyte injury model for in vitro mechanistic validation, while we also established an AH mouse model using the ethanol with gradually increased concentration of 2–4% (v/v) for in vivo study. Specific role of 1700020I14Rik/miR-137/AKR1B10 in AML12 cell viability, proliferation and apoptotic capacity as well as inflammation and liver damage in mice were analyzed following ectopic and depletion approaches. We found elevated AKR1B10 and 1700020I14Rik but reduced miR-137 in AH. 1700020I14Rik was able to elevated miR-137-mediated AKR1B10. In vitro cell experiments and in vivo animal experiments validated that 1700020I14Rik reduced ethanol-induced hepatocyte damage and inflammation in AH mice through regulation of miR-137–mediated AKR1B10/Erk axis. The current study underlied that 1700020I14Rik could activate AKR1B10/Erk signaling through inhibition of miR-137, thereby promoting the hepatocyte damage in AH mice.

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AKR1B10 inhibits the proliferation and migration of gastric cancer via regulating epithelial-mesenchymal transition

Cited by 15 publications

References 33 publications

Ferroptotic MSCs protect mice against sepsis via promoting macrophage efferocytosis

Ferroptotic MSCs protect mice against sepsis via promoting macrophage efferocytosis

Overexpression of AKR1B10 Predicts Poor Prognosis in Gastric Cancer Patients Undergoing Surgical Resection

LncRNA 1700020I14Rik promotes AKR1B10 expression and activates Erk pathway to induce hepatocyte damage in alcoholic hepatitis

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