&lt;p&gt;LncRNA-SNHG16 Silencing Inhibits Prostate Carcinoma Cell Growth, Downregulate GLUT1 Expression and Reduce Glucose Uptake&lt;/p&gt;

Shao, Mingfeng; Yu, Ziqiang; Zou, Jianan

doi:10.2147/cmar.s231370

Cited by 17 publications

(19 citation statements)

References 19 publications

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“…Moreover, lncRNAs are tightly associated with therapeutic options and prognostic values of cancer patients (6). Here we observed SNHG16 was positively associated with gastric cancer, consistently with previous reports (9,10). Results from this study indicate that SNHG16 is overexpressed in the tumor tissues of GC patients and high expression of SNHG16 is associated with poor prognosis.…”

Section: Discussionsupporting

confidence: 92%

“…For instance, studies reported that SNHG16 is high-expressed in colon cancer and regulated by the Wnt pathway (9). In addition, silencing SNHG16 inhibits prostate cell growth (10). Studies have uncovered a lncRNA-miRNA network where lncRNAs function as competitive endogenous RNAs (ceRNA) of miRNAs to recover the mRNA target genes expressions (11), suggesting the lncRNA-miRNA network is a potential target for anti-cancer therapy.…”

Section: Introductionmentioning

confidence: 99%

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Blocking lncRNA-SNHG16 Sensitizes Gastric Cancer Cells to 5-Fu Through Targeting the miR-506-3p-PTBP1-Mediated Glucose Metabolism

Ding

Gao

Zheng

et al. 2021

Preprint

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Gastric cancer (GC) is one of the most human malignancies. The 5-fluorouracil (5-Fu) is a first-line anti-gastric cancer chemotherapeutic agent. However, a large number of GC patients developed 5-Fu resistance. Currently, the biological roles and molecular mechanisms of lncRNA-SNHG16 in 5-Fu resistant gastric cancer still remain elusive. Here we report SNHG16 as well as PTBP1 are positively associated with 5-Fu resistance of gastric cancer. SNHG16 and PTBP1 are significantly upregulated in gastric tumors and cell lines. Silencing SNHG16 or PTBP1 effectively sensitized GC cells to 5-Fu. Furthermore, the glucose metabolism was remarkedly elevated in 5-Fu resistant GC cells. Under low glucose supply, 5-Fu resistant cells displayed higher vulnerability than parental GC cells. Bioinformatical analysis and luciferase assay demonstrated that SNHG16 downregulated miR-506-3p by sponging it. We identified PTBP1 was a direct target of miR-506-3p in GC cells. RNA-seq results indicated PTBP1 positively regulated multiple glycolysis enzymes expressions, including GLUT1, HK2 and LDHA. Bioinformatics analysis illustrated the 3’UTRs of glycolysis enzymes contained multiple PTBP1 binding sites, which were further verified by RNA-pull down and RNA immunoprecipitation assays. Consequently, we demonstrated PTBP1 upregulated the mRNAs of glycolysis enzymes via promoting the mRNAs stabilities. Finally, in vivo xenograft experiments validated that blocking the SNHG16-mediated miR-506-3p-PTBP1 axis effectively sensitized xenograft tumors to 5-Fu treatments. Summarily, our study reports biological roles and molecular mechanisms underlying the lncRNA SNHG16-mediated 5-Fu resistance in GC through modulating the miR-506-3p-PTBP1-glycolysis axis, presenting a promising prospect in improvement of 5-Fu therapy for chemoresistant GC patients.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Blocking lncRNA-SNHG16 Sensitizes Gastric Cancer Cells to 5-Fu Through Targeting the miR-506-3p-PTBP1-Mediated Glucose Metabolism

Ding

Gao

Zheng

et al. 2021

Preprint

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“…Recent research reports, SNHG16 over-expressed in PCa patients and play a role in promoting cell proliferation by regulating GLUT-1 expression and glucose uptake [10]. Here, we found SNHG16-incuded DU-145 cell proliferation, migration and invasion via up-regulating c-MYC, TGFBR2, E2F4, p-SMAD2, and p-SMAD3 expression.…”

Section: Discussionsupporting

confidence: 54%

“…1A). SNHG16 might play an important role in tumor progression [10]. In order to study the role of SNHG16 in PCa, we knocked down and overexpressed SNHG16 in DU-145 cells (Fig.…”

Section: The High Expression Of Snhg16 In Pca Tissues Promoted Tumor mentioning

confidence: 99%

“…LncRNA small-nucleolar RNA host gene 16 (SNHG16) was a novel tumor oncogene identi ed in many cancers. SNHG16 was found to be overexpressed in PCa patients, which promoted GLUT-1 expression to induce glucose uptake and PCa cell proliferation [10]. In cervical cancer, SNHG16 promoted tumor progression by directly targeted miR-216A-5p/ZEB1 axis [11].…”

Section: Introductionmentioning

confidence: 99%

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Long Noncoding RNA SNHG16 Functions as Tumor Activator by Sponging hsa-miR-373-3p to Regulate TGFBR2/SMAD Pathway in Prostate Cancer

Weng

Liu

et al. 2020

Preprint

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Background: Long noncoding RNAs (lncRNAs) are one of the major causes of tumorigenesis. However, the roles and mechanisms of lncRNA SNHG16 in prostate cancer (PCa) remain unknown. The purpose of this study was to elucidate the mechanisms of lncRNA SNHG16 in the proliferation and metastasis of human PCa cells.Material and Methods: First, the quantitative polymerase chain reaction (qPCR) was used to measure SNHG16 expression in PCa tissues and adjacent normal tissues (n=80). Down-regulate and over-express SNHG16 in human PCa DU-145 cell. Then cell proliferation was detected by CCK8 assay, cell apoptosis was analyzed by flow cytometry, cell migration were determined by wound healing, and cell invasion was examined by transwell. Western blot assays were used to examine the expression of the TGFBR2, c-MYC, E2F4, SMAD2, p-SMAD2, SMAD3, and p-SMAD3. Second, the targeting relationship between SNHG16 and hsa-miR-373-3p was verified by dual-luciferase reporter assay and rescue experiments. Third, the targeting relationship between hsa-miR-373-3p and TGFBR2 was verified by dual-luciferase reporter assay and rescue experiments. Results: The expression of SNHG16 was significant increase in PCa tissues (Z=-8.405, P<0.001), and with significant correlation with patient's age (<60 and ≥60 years old, P=0.007). Silencing SNHG16 inhibited DU-145 cell proliferation, migration, and invasion, while induced cell apoptosis significantly (P<0.01, respectively). Overexpressing SNHG16 promoted cell proliferation, migration and invasion, and reduced cell apoptosis rate (P<0.05, respectively). SNHG16 overexpression observably increased TGFBR2, c-MYC, E2F4, p-SMAD2, and p-SMAD3 expression (P<0.001, respectively), but SNHG16 inhibition was opposite. However, SNHG16 did not regulate SMAD2 and SMAD3 expression. Next, hsa-miR-373-3p was found down-regulated in PCa tissues (Z=-8.344, P<0.001), and the down-regulation of hsa-miR-373-3p were closely linked to Gleason score (Gleason score: <7 and >7, P = 0.024). Hsa-miR-373-3p expression of hsa-miR-373-3p was negatively correlated with SNHG16 (r=-0.544, P<0.001). The result of dual-luciferase reporter assay and qPCR test revealed that hsa-miR-373-3p was a target of SNHG16. Hsa-mir-373-3p inhibitor could rescue sh-SNHG16-inhibited cell proliferation, migration and invasion by promoting TGFBR2, C-MYC, E2F4, P-Smad2, and P-smad3 expression. Finally, we found that TGFBR2 may be the target gene of hsa-mir-373-3p through TargetScan and starbase. Further research found that TGFBR2 was markedly up-regulated in PCa tissues (Z=-5.945, P<0.001), and the expression of TGFBR2 was negatively correlated with hsa-miR-373-3p (r=-0.627, P<0.001). Dual-luciferase reporter assay and qPCR test showed that TGFBR2 was a target of hsa-miR-373-3p. TGFBR2 knockdown could inhibit hsa-mir-373-3p inhibitor-induced cell proliferation, migration and invasion, and reversed the effect of hsa-mir-373-3p inhibitor on cell apoptosis. Based on the data, sh-TGFBR2 partially disabled hsa-mir-373-3p inhibitor effect. Conclusion: LncRNA SNHG16 might act as a ceRNA to regulate the proliferation and migration of DU-145 cells by modulating the hsa-miR-373-3p/TGFBR2/SMAD axis.

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Advancements in long non-coding RNA-based therapies for cancer: targeting, delivery, and clinical implications

Ammad,

Javed,

Sadia

et al. 2024

Med Oncol

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<p>LncRNA-SNHG16 Silencing Inhibits Prostate Carcinoma Cell Growth, Downregulate GLUT1 Expression and Reduce Glucose Uptake</p>

Cited by 17 publications

References 19 publications

Blocking lncRNA-SNHG16 Sensitizes Gastric Cancer Cells to 5-Fu Through Targeting the miR-506-3p-PTBP1-Mediated Glucose Metabolism

Blocking lncRNA-SNHG16 Sensitizes Gastric Cancer Cells to 5-Fu Through Targeting the miR-506-3p-PTBP1-Mediated Glucose Metabolism

Long Noncoding RNA SNHG16 Functions as Tumor Activator by Sponging hsa-miR-373-3p to Regulate TGFBR2/SMAD Pathway in Prostate Cancer

Advancements in long non-coding RNA-based therapies for cancer: targeting, delivery, and clinical implications

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<p>LncRNA-SNHG16 Silencing Inhibits Prostate Carcinoma Cell Growth, Downregulate GLUT1 Expression and Reduce Glucose Uptake</p>

Cited by 17 publications

References 19 publications

Blocking lncRNA-SNHG16 Sensitizes Gastric Cancer Cells to 5-Fu Through Targeting the miR-506-3p-PTBP1-Mediated Glucose Metabolism

Blocking lncRNA-SNHG16 Sensitizes Gastric Cancer Cells to 5-Fu Through Targeting the miR-506-3p-PTBP1-Mediated Glucose Metabolism

Long Non­coding RNA SNHG16 Functions as Tumor Activator by Sponging hsa-miR-373-3p to Regulate TGFBR2/SMAD Pathway in Prostate Cancer

Advancements in long non-coding RNA-based therapies for cancer: targeting, delivery, and clinical implications

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Long Noncoding RNA SNHG16 Functions as Tumor Activator by Sponging hsa-miR-373-3p to Regulate TGFBR2/SMAD Pathway in Prostate Cancer