Knockdown of High Mobility Group-Box 3 (HMGB3) Expression Inhibits Proliferation, Reduces Migration, and Affects Chemosensitivity in Gastric Cancer Cells

Guo, Shengnan; Wang, Yuanyuan; Gao, Yu; Zhang, Yinxu; Chen, Mingzi; Xu, Minghao; Hu, Lu; Yu, Jing; Jing, Fangyu; Li, Chen; Wang, Qingjun; Zhu, Zhou

doi:10.12659/msm.900880

Cited by 31 publications

(26 citation statements)

References 32 publications

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“…HMGB3 has been suggested to promote initiation and progression of multiple cancer. 38,39 In addition, Yamada et al revealed that HMGB3 mRNA expression was obviously enhanced in PCa tissues and its knockdown limited PCa cell growth, migration, and invasion. 18 In this article, the data presented that HMGB3 mRNA and protein abundance were enhanced in PCa tissues and cells.…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA SOX2-OT Knockdown Inhibits Proliferation and Metastasis of Prostate Cancer Cells Through Modulating the miR-452-5p/HMGB3 Axis and Inactivating Wnt/β-Catenin Pathway

Song

Wang

et al. 2020

Cancer Biotherapy and Radiopharmaceuticals

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Background: Recent studies have proven that abnormal expression of long noncoding RNAs (lncRNAs) often contributes to growth and invasion of cancer cells. The purpose of this study was to investigate the biological function and regulatory mechanism of lncRNA SOX2 overlapping transcript (SOX2-OT) in prostate cancer (PCa) progression. Materials and Methods: The expression of SOX2-OT, microRNA-452-5p (miR-452-5p), and high mobility group box 3 (HMGB3) was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Flow cytometry was performed to determine the cell cycle distribution. Western blot assay was conducted to measure the protein levels of cyclin D1, p21, p27, E-cadherin, vimentin, and N-cadherin. The interaction between miR-452-5p and SOX2-OT or HMGB3 was predicted by bioinformatics analysis and verified by dual-luciferase reporter assay and RNA immunoprecipitation assay. The mice xenograft model was established to investigate the role of SOX2-OT in vivo. Results: SOX2-OT and HMGB3 were upregulated, whereas miR-452-5p was downregulated in PCa tissues and cells. Knockdown of SOX2-OT inhibited PCa cell growth and metastasis. MiR-452-5p could directly bind to SOX2-OT and its knockdown reversed the inhibitory effects of SOX2-OT interference on growth and metastasis of PCa cells. HMGB3 was a direct target of miR-452-5p and its knockdown weakened the promotive effects of miR-452-5p silence on growth and metastasis of PCa cells. Moreover, HMGB3 expression was inversely regulated by miR-452-5p and positively modulated by SOX2-OT. Furthermore, SOX2-OT activated the Wnt/b-catenin signaling pathway through increasing HMGB3 expression. Finally, SOX2-OT knockdown hindered tumor growth in vivo by regulating miR-452-5p/HMGB3 axis. Conclusions: SOX2-OT downregulation limited PCa cell growth and metastasis by regulating miR-452-5p/ HMGB3 axis and inactivating Wnt/b-catenin signaling pathway, which might offer lncRNA-directed diagnosis and therapy for PCa.

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Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA SOX2-OT Knockdown Inhibits Proliferation and Metastasis of Prostate Cancer Cells Through Modulating the miR-452-5p/HMGB3 Axis and Inactivating Wnt/β-Catenin Pathway

Song

Wang

et al. 2020

Cancer Biotherapy and Radiopharmaceuticals

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“…Moreover, the dysregulation of HMGB3 has been found in many human cancers. For example, upregulation of HMGB3 was identified in gastric cancer, and knockdown of HMGB3 inhibited proliferation and migration of gastric cancer cells [12]. Moreover, overexpression of HMGB3 promoted cell proliferation, migration and was associated with poor prognosis in urinary bladder cancer patients [13].…”

Section: Introductionmentioning

confidence: 99%

LncRNA SNHG5 promotes nasopharyngeal carcinoma progression by regulating miR-1179/HMGB3 axis

et al. 2020

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Background: Long noncoding RNAs (lncRNAs) have been reported to be important regulators in pathogenesis of human cancers, including nasopharyngeal carcinoma (NPC). Here, we mainly aimed to explore the mechanisms of LncRNA-SNHG5/ miR-1179/HMGB3 axis in NPC progression. Methods: RT-qPCR and Western blot analysis were employed to detect mRNA and protein expressions. CCK-8, Transwell and dual luciferase reporter assays were applied to investigate functions of LncRNA-SNHG5/miR-1179/ HMGB3 axis. Results: Upregulation of lncRNA-SNHG5 and downregulation of miR-1179 were identified in NPC, which were associated with adverse clinical outcomes. Functionally, upregulation of lncRNA-SNHG5 and downregulation of miR-1179 accelerated NPC cell proliferation, migration and invasion. Furthermore, lncRNA-SNHG5 acted as a molecular sponge of miR-1179 in NPC. Besides that, upregulation of HMGB3 was found in NPC, and knockdown of HMGB3 restrained NPC progression. Moreover, HMGB3, a target of miR-1179, regulated NPC progression by mediating LncRNA-SNHG5/miR-1179 axis. Conclusion: LncRNA SNHG5 serves as a tumor promoter in NPC by sponging miR-1179 and upregulating HMGB3.

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“…miR-429 is a member of the miR-200 family, and we previously reported the tumor suppressive role of miR-429 in colon cancer cell lines (11). High mobility group box 3 (HMGB3) has been reported to be an oncogene (12)(13)(14)(15). However, to the best of our knowledge, the molecular mechanisms underlying the association between miR-429 and HMGB3 in CRC are yet to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑429 acts as a tumor suppressor in colorectal cancer by targeting high mobility group box 3

Tian

Chang

Wu³

et al. 2021

Oncol Lett

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Colorectal cancer (CRC) is one of the most common solid tumors worldwide and has an extremely poor prognosis. MicroRNA-429 (miR-429) has been reported to participate in the progression of CRC. However, the pathological mechanisms require further investigation. The aim of the present study was to investigate the association between miR-429 and high mobility group box 3 (HMGB3) in CRC and the associated mechanism. The mRNA expression levels of miR-429 and HMGB3 in 65 paired CRC and adjacent tissues were examined by reverse transcription-quantitative PCR. Furthermore, a dual-luciferase reporter assay was performed to identify the association between miR-429 and HMGB3. Finally, the effects of miR-429 and HMGB3 on the proliferation and apoptosis of CRC cells were detected. As a result, it was identified that miR-429 expression was downregulated and HMGB3 expression was upregulated in CRC tissues compared with in adjacent non-cancer tissues, and the expression levels of miR-429 were negatively associated with those of HMGB3. Notably, HMGB3 was demonstrated to be a direct target of miR-429 by dual-luciferase reporter assay. Furthermore, transfection with a miR-429 mimic significantly inhibited HMGB3 expression and led to decreased proliferation and increased apoptosis of CRC cells. On the other hand, transient overexpression of HMGB3 partially inhibited the antitumor effects of miR-429. To the best of our knowledge, the present study demonstrated for the first time that miR-429 regulated the proliferation and apoptosis of CRC cells via HMGB3, suggesting a specific tumor suppressive function of the miR-429/HMGB3 signaling pathway in CRC.

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Knockdown of High Mobility Group-Box 3 (HMGB3) Expression Inhibits Proliferation, Reduces Migration, and Affects Chemosensitivity in Gastric Cancer Cells

Cited by 31 publications

References 32 publications

Long Noncoding RNA SOX2-OT Knockdown Inhibits Proliferation and Metastasis of Prostate Cancer Cells Through Modulating the miR-452-5p/HMGB3 Axis and Inactivating Wnt/β-Catenin Pathway

Long Noncoding RNA SOX2-OT Knockdown Inhibits Proliferation and Metastasis of Prostate Cancer Cells Through Modulating the miR-452-5p/HMGB3 Axis and Inactivating Wnt/β-Catenin Pathway

LncRNA SNHG5 promotes nasopharyngeal carcinoma progression by regulating miR-1179/HMGB3 axis

MicroRNA‑429 acts as a tumor suppressor in colorectal cancer by targeting high mobility group box 3

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