HMGB1 Promotes the Proliferation and Metastasis of Lung Cancer by Activating the Wnt/β-Catenin Pathway

Wang, Xiaohui; Zhang, Shuying; Xu, Xiaopeng

doi:10.1177/1533033820948054

Cited by 25 publications

(15 citation statements)

References 18 publications

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“…In recent years, many studies have focused on its role in a variety of cancers, including CRC. Various reports have shown that HMGB1 expression is significantly upregulated in breast cancer, gastric cancer, lung cancer and other cancers and downregulated in pancreatic cancer [ 27 – 30 ]. Researchers have reported that HMGB1 may regulate the reactivity of rectal cancer cells to preoperative chemoradiotherapy [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

miR-495-3p depresses cell proliferation and migration by downregulating HMGB1 in colorectal cancer

Zhang

Zheng

et al. 2022

World J Surg Onc

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Background MicroRNAs play an important role in the genesis and progression of tumours, including colorectal cancer (CRC), which has a high morbidity and mortality rate. In this research, the role of miR-495-3p and HMGB1 in CRC was investigated. Methods We performed qRT-PCR to detect the expression of miR-495-3p in colorectal cancer tissues and cell lines. Functional experiments, such as CCK-8, EdU, Transwell and apoptosis assays, were conducted to explore the effects of miR-495-3p on the proliferation, migration and apoptosis of CRC cells in vitro. Then, database prediction, dual-luciferase reporter gene assays and functional experiments verified the role of the miR-495-3p target gene HMGB1 in CRC. Finally, rescue experiments were performed to investigate whether overexpression of HMGB1 could reverse the inhibitory effect of miR-495-3p on CRC cell proliferation in vivo and in vitro. Results miR-495-3p was downregulated in colorectal cancer tissues and cell lines, inhibited the proliferation and migration of colorectal cancer cells and promoted cell apoptosis. Database prediction and dual-luciferase reporter gene assays showed that HMGB1 was the downstream target gene of miR-495-3p. We finally demonstrated that miR-495-3p inhibited CRC cell proliferation by targeting HMGB1 in vitro and in vivo. Conclusion Our research shows that miR-495-3p inhibits the progression of colorectal cancer by downregulating the expression of HMGB1, which indicates that miR-495-3p may become a potential therapeutic target for colorectal cancer.

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Section: Discussionmentioning

confidence: 99%

miR-495-3p depresses cell proliferation and migration by downregulating HMGB1 in colorectal cancer

Zhang

Zheng

et al. 2022

World J Surg Onc

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“…HMGB1 has been shown to be involved in inflammatory and oxidative stress and apoptosis through multiple signaling pathways including WNT, Keap1/Nrf2/ARE, and PI3K/AKT [ 36 – 38 ]. Furthermore, previous studies have confirmed the role of the ROS/NF- κ B pathway in activating HMGB1 in TDI-induced inflammatory injury [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

lncRNA HOTAIR Inhibition by Regulating HMGB1/ROS/NF-κB Signal Pathway Promotes the Recovery of Spinal Cord Function

Wang

Long

Yang

et al. 2022

Computational and Mathematical Methods in Medicine

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Spinal cord ischemia-reperfusion injury (SCII) is one of the most serious complications of clinical aortic aneurysm and vascular malformation surgery. Long noncoding RNA (lncRNA) is involved in the progression of SCII, whereas long noncoding RNA HOX transcript antisense RNA (lncRNA HOTAIR) is unclear in SCII. This study is aimed at confirming the role and related mechanism of HOTAIR in SCII. Later on, a model of SCII was established by clamping the aortic arch for 14 minutes. RNA expression of HOTAIR was detected via qRT-PCR at 12 h, 24 h, 36 h, and 48 h after SCII. The Tarlov scoring system and TUNEL assay were used to evaluate neurological function and neuronal apoptosis. Oxidative stress factor levels were assessed according to the instructions of the kit. Inflammatory cytokines were assessed by ELISA. Western blot was used to detect levels of p65, p-p65, I-κBα, and p-I-κBα. We found HOTAIR was raised in SCII rats. si-HOTAIR was able to reverse SCII-induced oxidative stress in SCII rats. The HMGB1 expression was upregulated in SCII tissues and negatively correlated with HOTAIR. HMGB1 was able to partially reverse si-HOTAIR inhibition of oxidative stress, inflammatory injury, and neuronal cell apoptosis in SCII. In addition, the ROS/NF-κB signaling pathway is involved in HOTAIR/HMGB1 regulation of SCII. In a word, HOTAIR inhibition is able to inhibit oxidative stress, inflammatory injury, and neuronal apoptosis in SCII through downregulation of the high mobility group protein B1(HMGB1), which is achieved by inhibiting the ROS/NF-κB signaling pathway. The HOTAIR/HMGB1/ROS/NF-κB molecular pathway may be a new mechanism for the treatment of SCII.

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“…Platelet HMGB1 has been implicated in thrombosis, inflammation, and platelet activation involving TLR4/RAGE [ 39 , 41 ]. Tumor HMGB1 and TLR4/RAGE receptors promote cell proliferation, survival, migration, epithelial-to-mesenchymal transition, and apoptosis resistance involving interaction with β-catenin, Runx2, YAP1, and TGF-β1/Smad [ 38 , 42 , 43 , 44 , 45 , 46 ]. However, HMGB1 released from dying tumor cells may stimulate bone marrow-derived tumor-infiltrating myeloid dendritic cells through HMGB1/TLR2 signaling [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

Exosomal HMGB1 Promoted Cancer Malignancy

Wang

Lin

et al. 2021

Cancers

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Reciprocal crosstalk between platelets and malignancies underscores the potential of antiplatelet therapy in cancer treatment. In this study, we found that human chronic myeloid leukemia K562 cell-differentiated megakaryocytes and murine platelets produced bioactive substances and these are released into the extracellular space, partly in their exosomal form. High-mobility group box 1 (HMGB1) is a type of exosomal cargo, and the antiplatelet drugs aspirin and dipyridamole interfered with its incorporation into the exosomes. Those released substances and exosomes, along with exogenous HMGB1, promoted cancer cell survival and protected cells from doxorubicin cytotoxicity. In a tumor-bearing model established using murine Lewis lung carcinoma (LLC) cells and C57BL/6 mice, the tumor suppressive effect of dipyridamole correlated well with decreased circulating white blood cells, soluble P-selectin, TGF-β1 (Transforming Growth Factor-b1), exosomes, and exosomal HMGB1, as well as tumor platelet infiltration. Exosome release inhibitor GW4869 exhibited suppressive effects as well. The suppressive effect of dipyridamole on cancer cell survival was paralleled by a reduction of HMGB1/receptor for advanced glycation end-products axis, and proliferation- and migration-related β-catenin, Yes-associated protein 1, Runt-related transcription factor 2, and TGF- β1/Smad signals. Therefore, exosomes and exosomal HMGB1 appear to have roles in platelet-driven cancer malignancy and represent targets of antiplatelet drugs in anticancer treatment.

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HMGB1 Promotes the Proliferation and Metastasis of Lung Cancer by Activating the Wnt/β-Catenin Pathway

Cited by 25 publications

References 18 publications

miR-495-3p depresses cell proliferation and migration by downregulating HMGB1 in colorectal cancer

miR-495-3p depresses cell proliferation and migration by downregulating HMGB1 in colorectal cancer

lncRNA HOTAIR Inhibition by Regulating HMGB1/ROS/NF-κB Signal Pathway Promotes the Recovery of Spinal Cord Function

Exosomal HMGB1 Promoted Cancer Malignancy

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