NDRG3 facilitates colorectal cancer metastasis through activating Src phosphorylation

Li, Ting; Sun, Ruochuan; Lu, Mingdian; Chang, Jun; Meng, Xiang-Ling; Wu, Hongmei

doi:10.2147/ott.s156814

Cited by 12 publications

(16 citation statements)

References 32 publications

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“…Next, we attempted to identify the genes regulated by miR‐122‐5p and the luciferase assays verified that NDRG3 was one of its targets. NDRG3 is considered an oncogene in hepatocellular carcinoma and colorectal cancer 53,54 . By performing a series of experiments, we identified that NDRG3 was upregulated in OS tissues and cell lines.…”

Section: Discussionmentioning

confidence: 99%

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The LINC01410/miR‐122‐5p/NDRG3 axis is involved in the proliferation and migration of osteosarcoma cells

Zhao

Xue

et al. 2021

IUBMB Life

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It is generally accepted that long noncoding RNAs (lncRNAs) function as vital regulators of tumor development and progression. Long intergenic non-coding RNA 1410 (LINC01410) is a newly discovered lncRNA, and its role in osteosarcoma (OS) is yet to be determined. Materials and methods: The expression of LINC01410, microRNA-122-5p (miR-122-5p), and N-myc downstream-regulated gene 3 (NDRG3) in OS tissues was determined using reverse transcription-quantitative PCR. Interactions between LINC01410, miR-122-5p, and NDRG3 were predicted and verified using bioinformatics tools and luciferase assays. Cell proliferation, migration, and invasion were detected using cell counting Kit-8 and Transwell assays. Results: LINC01410 was overexpressed in OS tissues. Furthermore, it was confirmed that LINC01410 facilitated OS cell proliferation and migration. Our studies also showed that LINC01410 binds to miR-122-5p, and miR-122-5p binds to NDRG3. Finally, we observed that LINC01410 knockdown inhibited the proliferation, invasion, and migration of OS cells. Knockdown of LINC01410 resulted in the upregulation of miR-122-5p and downregulation of NDRG3. Conclusion: Our results demonstrated that the LINC01410/miR-122-5p/ NDRG3 axis is involved in the progression of OS.

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Section: Discussionmentioning

confidence: 99%

“…NDRG3 is considered an oncogene in hepatocellular carcinoma and colorectal cancer. 53,54 By performing a series of experiments, we identified that…”

Section: Discussionmentioning

confidence: 99%

The LINC01410/miR‐122‐5p/NDRG3 axis is involved in the proliferation and migration of osteosarcoma cells

Zhao

Xue

et al. 2021

IUBMB Life

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“…Then a pro-tumorigenic activity was reported for a member of the NDRG family, NDRG3, when it was known to be associated with prostate cancer [23]. Later, in the last five years of studies have elucidated additional roles of NDRG3 in various hypoxia responses, including cell proliferation, double-strand break repair, metastasis, and HIF regulation [24][25][26][27][28][29]. In this study, we determined the crystal structure of a truncated human NDRG3 fragment comprising residues from 29 to 320 (NDRG3 ΔNC), on the basis of its solubility and crystallizability.…”

Section: Discussionmentioning

confidence: 99%

“…In lieu of the lactate-mediated NDRG3 signaling, NDRG3 provokes anti-apoptotic processes during the hypoxia postcondition by regulating adenosine A2a receptors [26], activates Src phosphorylation in colorectal cancer progression [27], and promotes hepatocellular carcinoma metastasis via regulating turnover of β-catenin [28]. On the other hand, NDRG3 is involved in anti-metastatic functions, by dissociating the coactivator p300 from HIF-1a [29].…”

Section: Introductionmentioning

confidence: 99%

Structural and Biophysical Analyses of Human N-Myc Downstream-Regulated Gene 3 (NDRG3) Protein

Kim

Park

et al. 2020

Biomolecules

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The N-Myc downstream-regulated gene (NDRG) family belongs to the α/β-hydrolase fold and is known to exert various physiologic functions in cell proliferation, differentiation, and hypoxia-induced cancer metabolism. In particular, NDRG3 is closely related to proliferation and migration of prostate cancer cells, and recent studies reported its implication in lactate-triggered hypoxia responses or tumorigenesis. However, the underlying mechanism for the functions of NDRG3 remains unclear. Here, we report the crystal structure of human NDRG3 at 2.2 Å resolution, with six molecules in an asymmetric unit. While NDRG3 adopts the α/β-hydrolase fold, complete substitution of the canonical catalytic triad residues to non-reactive residues and steric hindrance around the pseudo-active site seem to disable the α/β-hydrolase activity. While NDRG3 shares a high similarity to NDRG2 in terms of amino acid sequence and structure, NDRG3 exhibited remarkable structural differences in a flexible loop corresponding to helix α6 of NDRG2 that is responsible for tumor suppression. Thus, this flexible loop region seems to play a distinct role in oncogenic progression induced by NDRG3. Collectively, our studies could provide structural and biophysical insights into the molecular characteristics of NDRG3.

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“…In addition, NDRG family members are tumor-associated proteins and their dysregulation may result in tumorigenesis (5). NDRG3 has been reported to promote colorectal cancer metastasis by activating Src phosphorylation (6), and is associated with poor survival in non-small cell lung cancer (7). However, the role of NDRG3 and regulatory mechanisms of NDRG3 in gastric cancer remain unclear.…”

Section: Introductionmentioning

confidence: 99%

SNHG20/miR‑140‑5p/NDRG3 axis contributes to 5‑fluorouracil resistance in gastric cancer

Shen

et al. 2019

Oncol Lett

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5-fluorouracil (5-FU)-based chemotherapy is the first line treatment for advanced gastric cancer. However, the effectiveness of 5-FU is limited by drug resistance. The N-myc downstream-regulated gene, family member 3 (NDRG3) is a member of the NDRG family and has been implicated in numerous types of cancer. However, the role of NDRG3 in gastric cancer remains unclear. In the present study, NDRG3 mRNA expression in gastric cancer and adjacent normal tissues was analyzed using the Gene Expression Profiling Interactive Analysis web tool. NDRG3 expression was silenced using short hairpin RNAs to examine the effect of NDRG3 on the growth of gastric cancer cells. Potential regulators of NDRG3 were identified using the TargetScan and MicroRNA tools and verified by a luciferase assay and reverse transcription-quantitative PCR analysis. The current study demonstrated that NDRG3 was upregulated in gastric cancer specimens and promoted cell proliferation in gastric cancer cell lines. Furthermore, the present study revealed that the small nucleolar RNA host gene 20 (SNHG20)/microRNA (miR)-140-5p signaling pathway may regulate the expression of NDRG3. SNHG20 was revealed to be involved in mediating resistance to 5-FU in gastric cancer cell lines via NDRG3. In conclusion, the results of the present study suggest that the SNHG20/miR-140-5p/NDRG3 axis may be involved in mediating resistance to 5-FU in gastric cancer.

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NDRG3 facilitates colorectal cancer metastasis through activating Src phosphorylation

Cited by 12 publications

References 32 publications

The LINC01410/miR‐122‐5p/NDRG3 axis is involved in the proliferation and migration of osteosarcoma cells

The LINC01410/miR‐122‐5p/NDRG3 axis is involved in the proliferation and migration of osteosarcoma cells

Structural and Biophysical Analyses of Human N-Myc Downstream-Regulated Gene 3 (NDRG3) Protein

SNHG20/miR‑140‑5p/NDRG3 axis contributes to 5‑fluorouracil resistance in gastric cancer

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