MiR-4521 plays a tumor repressive role in growth and metastasis of hepatocarcinoma cells by suppressing phosphorylation of FAK/AKT pathway via targeting FAM129A

Ayesha, Munawar; Majid, Abbasi; Zhao, Dongting; Greenaway, Frederick T.; Yan, Naimeng; Liu, Qinglong; Liu, Shuqing; Sun, Ming‐Zhong

doi:10.1016/j.jare.2021.05.003

Cited by 17 publications

(14 citation statements)

References 65 publications

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Section: Discussionmentioning

confidence: 99%

“…26 Elevated MDM2 inhibits P53 transcriptional activity by promoting its degradation, resulting in cancer progression. 27 p-AKT was reported to promote proliferation via the MDM2/P53 pathway and inhibit apoptosis via the BCL-2/BAX/Cytochrome-C/Caspase-3/Caspase-9 pathway; it promoted invasion and migration via Snail/ E-cadherin/N-cadherin/Vimentin pathway. 27 Oncogenic AKT induces the transcription of CCND1, CCND2, and CDK4 to regulate G1-S cell cycle transition.…”

Section: Discussionmentioning

confidence: 99%

“…27 p-AKT was reported to promote proliferation via the MDM2/P53 pathway and inhibit apoptosis via the BCL-2/BAX/Cytochrome-C/Caspase-3/Caspase-9 pathway; it promoted invasion and migration via Snail/ E-cadherin/N-cadherin/Vimentin pathway. 27 Oncogenic AKT induces the transcription of CCND1, CCND2, and CDK4 to regulate G1-S cell cycle transition. 22 P27 is repressed by AKT and enhanced by p53 during the regulation of G1-S cell cycle transition.…”

Section: Discussionmentioning

confidence: 99%

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Silencing of FAM111B inhibits tumor growth and promotes apoptosis by decreasing AKT activity in ovarian cancer

Wang

et al. 2023

Exp Biol Med (Maywood)

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Ovarian cancer is the most lethal gynecological tumor in women worldwide. FAM111B (family with sequence similarity 111 member B) is an oncoprotein associated with multiple cancers, but its biological functions in ovarian cancer remain elusive. In this study, FAM111B was overexpressed in ovarian cancer tissues and cell lines. Functional studies in vitro revealed that silencing of FAM111B inhibited ovarian cancer cell proliferation, invasion, and migration, as well as increased cell apoptosis. Furthermore, FAM111B silencing arrested the ovarian cancer cell cycle at the G1/S phase. Furthermore, western blot assays demonstrated that silencing of FAM111B resulted in downregulation of phospho-AKT (p-AKT) protein expression, as well as upregulation of p53 and caspase-1 protein expression. The xenograft animal model of ovarian cancer demonstrated that FAM111B silencing inhibited tumor growth, enhanced cell apoptosis, and inhibited Ki-67 and proliferating cell nuclear antigen (PCNA) protein expression in vivo. Conversely, the overexpression of FAM111B exhibited opposite effects on the ovarian cancer xenograft. It was previously established that inactivating AKT inhibited ovarian cancer progression. This study found that silencing of FAM111B inhibits tumor growth and promotes apoptosis by decreasing AKT activity in ovarian cancer. Caspase-1 and p53 signaling also influenced the function of FAM111B in SKOV3 cells. Collectively, our results demonstrate that silencing of FAM111B is a potential therapeutic strategy against ovarian cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Silencing of FAM111B inhibits tumor growth and promotes apoptosis by decreasing AKT activity in ovarian cancer

Wang

et al. 2023

Exp Biol Med (Maywood)

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“…qRT-PCR was carried out using SYBR Green Master (ROX) (Roche, USA). The mRNA levels were calculated relative to the control Gapdh (for mRNA) or U6 (for miRs) using the 2 −ΔΔCq method, as previously reported [ 25 ].…”

Section: Methodsmentioning

confidence: 99%

Lean adipose tissue macrophage derived exosome confers immunoregulation to improve wound healing in diabetes

et al. 2023

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Chronic non-healing wounds, a prevalent complication of diabetes, are associated with increased mortality in diabetic patients. Excessive accumulation of M1 macrophages in diabetic wounds promotes inflammation and results in dysregulated tissue repair. Adipose tissue macrophages (ATMs) derived from healthy lean donors have the ability to improve glucose tolerance and insulin sensitivity, as well as modulate inflammation. MicroRNAs (miRs), which can be packaged into exosomes (Exos) and secreted from cells, serve as essential regulators of macrophage polarization. Here, we revealed that ATMs isolated from lean mice secrete miRs-containing Exos, which modulate macrophage polarization and promote rapid diabetic wound healing when administered to diabetes-prone db/db mice. The miRs sequence of tissue samples from wounds treated with Exos secreted by lean ATMs (ExosLean) revealed that miR-222-3p was up-regulated. Further analyses showed that inhibiting miR-222-3p using a miR inhibitor impaired the macrophage-reprogramming effect of ExosLean. In the excisional skin wound mouse model, locally inhibiting miR-222-3p disrupted healing dynamics and failed to modulate macrophage polarization. Mechanistic studies revealed a connection between miR-222-3p, Bcl2l11/Bim, an inflammatory response effector, macrophage polarization, and diabetic wound healing. In summary, ExosLean act as positive regulators of macrophage polarization by regulating miR levels in wounds and accelerating wound healing, and thus have important implications for wound management in diabetes. Graphic Abstract

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“…qRT-PCR was carried out using SYBR Green Master (ROX) (Roche, USA). The mRNA levels were calculated relative to the control Gapdh (for mRNA) or U6 (for miRNA) using the 2 −ΔΔCq method, as previously reported [25].…”

Section: Microrna Sequencingmentioning

confidence: 99%

Lean Adipose Tissue Macrophage Derived Exosome Confers Immunoregulation to Improve Wound Healing in Diabetes

Xia

Liu

Jiang

et al. 2022

Preprint

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Chronic non-healing wounds, an important complication of diabetes, are associated with increased mortality in patients afflicted with this disease. Excessive accumulation of M1 macrophages in diabetic wounds promotes inflammation and results in dysregulated tissue repair. Adipose tissue macrophages (ATMs) derived from healthy lean donors have the abilities to improve glucose tolerance and insulin sensitivity, and modulate inflammation. MiRNAs (miRs), which can be packaged into exosomes (Exos) and secreted from cells, serve as essential regulators of macrophage polarization. Here, we reveal that adipose tissue macrophages (ATMs) isolated from lean mice secrete miR-containing Exos, which modulate macrophage polarization and promote rapid diabetic wound healing when administered to diabetes-prone db/db mice. MiRs sequence of tissue samples from wounds treated with Exos secreted by lean ATMs (ATM-Exos) revealed that miR-222-3p was upregulated. Further analyses showed that inhibition of miR-222-3p using miR inhibitor impaired the macrophage-reprogramming effect of lean ATM-Exos. In the excisional skin wound mouse model, locally inhibiting miR-222-3p disrupted healing dynamics and failed to modulate macrophage polarization. Mechanistic studies revealed a link between miR-222-3p; Bcl2l11/Bim, an inflammatory response effector; macrophage polarization; and diabetic wound healing. In summary, lean ATM-Exos act as positive regulators of macrophage polarization by regulating miR levels in wounds and accelerating wound healing and thus have important implications for wound management in diabetes.

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MiR-4521 plays a tumor repressive role in growth and metastasis of hepatocarcinoma cells by suppressing phosphorylation of FAK/AKT pathway via targeting FAM129A

Cited by 17 publications

References 65 publications

Silencing of FAM111B inhibits tumor growth and promotes apoptosis by decreasing AKT activity in ovarian cancer

Silencing of FAM111B inhibits tumor growth and promotes apoptosis by decreasing AKT activity in ovarian cancer

Lean adipose tissue macrophage derived exosome confers immunoregulation to improve wound healing in diabetes

Lean Adipose Tissue Macrophage Derived Exosome Confers Immunoregulation to Improve Wound Healing in Diabetes

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