Long non‐coding <scp>RNA HCG11</scp> sponging <scp>miR</scp>‐522‐3p inhibits the tumorigenesis of non‐small cell lung cancer by upregulating <scp>SOCS5</scp>

Fan, Gang; Jen, Jin; Shen, Feng; Ren, Qingxia; Wang, Qing; Chu, Fulu

doi:10.1111/1759-7714.13624

Cited by 17 publications

(13 citation statements)

References 30 publications

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“…Multiple studies have found associations between SOCS5 expression levels and pathological conditions such as cancer. SOCS5 is upregulated in esophageal squamous cell carcinoma [ 22 ], liver cancer [ 23 ], non-small cell lung cancer [ 24 ], and prostate cancer [ 25 ]; hence, it is associated with specific biological characteristics of tumors. Moreover, SOCS5 partially reverses the inhibitory effect of miR-518c-3p on the invasion and migration of glioma cells [ 26 ].…”

Section: Introductionmentioning

confidence: 99%

SOCS5 contributes to temozolomide resistance in glioblastoma by regulating Bcl-2-mediated autophagy

Han

Yang

et al. 2022

Bioengineered

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Temozolomide (TMZ) is the primary chemotherapeutic drug for treating glioblastoma (GBM); however, the final clinical outcome is considerably limited by the poor response and resistance to TMZ. Although autophagy is thought to be associated with chemotherapy resistance and cancer cell survival, the precise molecular mechanisms underlying this process remain elusive. The suppressor of cytokine signaling (SOCS) family is widely distributed in vivo and exerts a range of effects on tumors; however, the expression pattern and role of SOCS in GBM remains unknown. In this study, we determined that high SOCS5 expression level was associated with poor prognosis and TMZ resistance in GBM. TMZ induced an increase in SOCS5 expression level and upregulated autophagy during the acquisition of drug resistance. The observed increase in the extent of autophagy was mediated by SOCS5. Mechanistically, SOCS5 enhances the transcription of Bcl-2. Knockdown of SOCS5 inhibited TMZ chemoresistance in GBM cells through the inhibition of Bcl-2 recruited autophagy; upregulation of Bcl-2 blocked this effect. In summary, our findings revealed the involvement and underlying mechanism of SOCS5 in TMZ resistance. SOCS5 plays a critical role in GBM chemoresistance and may serve as a novel prognostic marker and therapeutic target for chemotherapeutically treating drug-resistant GBM.

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Section: Introductionmentioning

confidence: 99%

SOCS5 contributes to temozolomide resistance in glioblastoma by regulating Bcl-2-mediated autophagy

Han

Yang

et al. 2022

Bioengineered

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“…Next, we also identified suppressor cytokine signaling-5 (SOCS5) was a negatively regulatory target of miR-522-3p using bioinformatics prediction and dual-luciferase assay. SOCS5 was also commonly found to be tumor-suppressed and significantly reduced in tumors, such as non-small cell lung cancer, pancreatic cancer and also liver cancer [ 43–45 ]. It was found that SOCS5 inhibition induced autophagy to impair metastasis in HCC cells via the PI3K/Akt/mTOR pathway [ 46 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA DHRS4-AS1 ameliorates hepatocellular carcinoma by suppressing proliferation and promoting apoptosis via miR-522-3p/SOCS5 axis

Zhou

Zou

et al. 2021

Bioengineered

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Recent years have seen much effect in revealing the pathological association between lncRNA and HCC. Herein, we identified lncRNA DHRS4-AS1 as a potential tumor suppressor in HCC. Firstly, it was discovered that DHRS4-AS1 was significantly down-regulated in HCC tissues compared to normal tissues based on the database TCGA. It was also detected in a lower-than-usual expression quantity in HCC tissues we collected and HCC cell lines. Kaplan-Meier survival analysis revealed that high expression of DHRS4-AS1 contributed to higher overall survival rate of HCC patients.DHRS4-AS1 expression was significantly correlated to tumor size ( P = 0.02) and TNM stage ( P = 0.045). CCK-8, BrdU and colony-forming assays collectively demonstrated that overexpression of DHRS4-AS1 significantly restrained HCC cell proliferation. In vivo xenograft animal experiment showed that DHRS4-AS1 could efficiently preclude the tumor growth of HCC. Further investigation performed using flow cytometry and western blot showed that DHRS4-AS1 exerted its effects by accelerating cell apoptosis and capturing cell cycle in G0/G1 phase. Our study subsequently lucubrated that miR-522-3p was a negative target of DHRS4-AS1. Increased expression level of miR-522-3p was examined in HCC tissues and cell lines. Similarly, miR-522-3p mimics could reverse the inhibitory effect on HCC brought by DHRS4-AS1. SOCS5 was then discovered as a down-stream target of miR-522-3p, which suggested that SOCS5 participated in DHRS4-AS1/miR-522-3p axis to collectively mediate the development of HCC. Our study provides lncRNA DHRS4-AS1/miR-522-3p/SOCS5 axis as a novel target for HCC therapeutic strategy with potentiality.

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“…SOCS5 expression is regulated by several miRNAs. miR-522-3p was found to directly target SOCS5 to promote lung cancer cell viability, migration and invasion (Fan et al, 2020). A recent study showed that SOCS5 was a direct target of miR-675-3p, which activated PI3K signaling to maintain pancreatic cancer cell stemness (Wang et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

Leonurine-Repressed miR-18a-5p/SOCS5/JAK2/STAT3 Axis Activity Disrupts CML malignancy

et al. 2021

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Leonurine, an active natural alkaloid compound isolated from Herba leonuri, has been reported to exhibit promising anticancer activity in solid tumors. The aim of this study was to explore whether leonurine is able to inhibit chronic myeloid leukemia (CML) malignancy. Here, we found that leonurine dose dependently inhibited the proliferation, migration, colony formation and promoted apoptosis of CML cells. Furthermore, leonurine markedly reduced CML xenograft growth in vivo. Mechanically, leonurine upregulated SOCS5 expression, thus leading JAK2/STAT3 signaling suppression. Silencing of SOCS5 by its siRNA abrogated the effect of leonurine on CML cells, demonstrating that SOCS5 mediates the anti-leukemia effect of leonurine. Notably, we observed that miR-18a-5p was remarkably increased in CML cells. Treating CML cells with leonurine significantly decreased miR-18a-5p expression. Moreover, we found miR-18a-5p repressed SOCS5 by directly targeting its 3′-UTR. miR-18a-5p downregulation induced by leonurine reduced the biological activity of CML cells by relieving miR-18a-5p repression of SOCS5 expression. Taken together, leonurine exerts significant anti-leukemia efficacy in CML by regulating miR-18a-5p/SOCS5/JAK2/STAT3 axis.

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Long non‐coding RNA HCG11 sponging miR‐522‐3p inhibits the tumorigenesis of non‐small cell lung cancer by upregulating SOCS5

Cited by 17 publications

References 30 publications

SOCS5 contributes to temozolomide resistance in glioblastoma by regulating Bcl-2-mediated autophagy

SOCS5 contributes to temozolomide resistance in glioblastoma by regulating Bcl-2-mediated autophagy

LncRNA DHRS4-AS1 ameliorates hepatocellular carcinoma by suppressing proliferation and promoting apoptosis via miR-522-3p/SOCS5 axis

Leonurine-Repressed miR-18a-5p/SOCS5/JAK2/STAT3 Axis Activity Disrupts CML malignancy

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