Increased lncRNA HOTAIR expression promotes the chemoresistance of multiple myeloma to dexamethasone by regulating cell viability and apoptosis by mediating the JAK2/STAT3 signaling pathway

Guan, Rongyan; Wang, Wei; Fu, Bin; Pang, Yanwei; Lou, Ye; Li, Hong

doi:10.3892/mmr.2019.10603

Cited by 16 publications

(12 citation statements)

References 32 publications

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“…A single lncRNA can act via multiple signaling pathways. For example, lncRNA HOTAIR acts through miR-204-5p/HMGB1 axis [ 40 ], miR-519a-3p/RRM1 axis [ 41 ], miR-601/ZEB1 axis [ 42 ], JAK2/STAT3 [ 43 ], hexokinase-2 [ 44 ], PI3K/Akt/mTOR [ 45 ] among other pathways. PlncRNA-1, is a newly identified lncRNA located on human chromosome 21 [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA PlncRNA-1 accelerates the progression of prostate cancer by regulating PTEN/Akt axis

Cui

Gao

Ning

et al. 2021

Aging

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Long non-coding RNAs are key regulators of tumor development and progression, with the potential to be biomarkers of tumors. This study aimed to explore the role of PlncRNA-1 in the progression of prostate cancer (PCa). We found that PlncRNA-1 was up-regulated in 85.29% of PCa tissues and could predict the T stage of PCa patients to a certain extent. Results showed that inhibition of PlncRNA-1 expression potentially promoted cell apoptosis, suppressed the proliferation, migration, and invasion of cells, and triggered G2/M cycle arrest in vitro and in vivo . PlncRNA-1 was mainly localized in the nucleus and PlncRNA-1 expression and phosphatase and tensin homologue (PTEN) expression were negatively correlated. Mechanistically, knockdown of PlncRNA-1 increased expression levels of PTEN protein and phosphorylated PTEN protein, and decreased expression levels of Akt protein and phosphorylated Akt protein. Rescue experiments demonstrated that PTEN inhibitors abolished the changes in PTEN/Akt pathway caused by PlncRNA-1 interference. PlncRNA-1 can promote the occurrence and development of PCa via the PTEN/Akt pathway. PlncRNA-1 may, therefore, be a new candidate target for the treatment of PCa.

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Section: Discussionmentioning

confidence: 99%

LncRNA PlncRNA-1 accelerates the progression of prostate cancer by regulating PTEN/Akt axis

Cui

Gao

Ning

et al. 2021

Aging

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“…According to previous studies, the lncRNA, TUG1, contributes to the proliferation and migration of hepatocellular carcinoma cells in vivo by upregulating miR-144 via inactivation of the JAK2/ STAT3 pathway (35). Moreover, the lncRNA, HOTAIR, was found to promote multiple myeloma cell viability and increase chemoresistance to dexamethasone via the JAK2/ STAT3 signaling pathway (36). We are of the opinion that KCNQ1OT1 competitively binds to microRNAs and regulates the downstream oncogenes or signaling pathways.…”

Section: Discussionmentioning

confidence: 95%

KCNQ1OT1 lncRNA affects the proliferation, apoptosis, and chemoresistance of small cell lung cancer cells via the JAK2/ STAT3 axis

Zhu¹,

Shen²,

Chen³

et al. 2021

Ann Transl Med

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Background: Small cell lung cancer (SCLC) is a devastating and aggressive neuroendocrine carcinoma characterized by high cellular proliferation and early metastatic spread. Numerous studies have demonstrated that long noncoding RNAs (lncRNAs) can regulate tumor generation and development, including in SCLC.The current study aimed to assess the effect of the lncRNA, KCNQ1OT1, on the proliferation, apoptosis, and chemoresistance of SCLC and the potential underlying molecular mechanism.Methods: Matched chemo-resistant and sensitive cells were applied to RNA isolation and followed by expression profiling by microarray analysis and subsequent quantitative polymerase chain reaction (qPCR) validation. Cell viability and apoptosis were determined by Cell Counting Kit-8 and flow cytometry to examine the chemoresistance and apoptosis of KCNQ1OT1 knockdown with lentivirus-mediated RNA interference. Furthermore, cell proliferation was studied by colony formation, and invasion and migration were tested by Transwell cell invasion and wound-healing assays, respectively. A tumor xenograft model was established to determine the role of KCNQ1OT1 in tumor growth and chemoresistance in response to KCNQ1OT1 knockdown in vivo. Western blot analysis, qPCR, and immunohistochemistry were used to detect the levels of messenger RNA (mRNA) Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway-related markers.Results: Higher expression of KCNQ1OT1 was detected in SCLC chemo-resistant verso chemo-sensitive cells. Knockdown of KCNQ1OT1 inhibited SCLC cell viability and cloning ability, hindered cell migration and invasion, induced apoptosis in vitro, and suppressed tumor growth and chemoresistance in vivo, by activating the JAK2/STAT3 signaling pathway.Conclusions: This is the first study to indicate that lncRNA KCNQ1OT1 promotes cell proliferation and invasion, and prevents apoptosis of SCLC by activating the JAK2/STAT3 pathway.

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“…lncRNAs also can promote chemoresistance by regulating tumor cells' apoptosis and cell cycle. Guan et al have revealed that elevated levels of the lncRNA HOTAIR increase the chemoresistance of MM to dexamethasone by regulating apoptosis and cell viability by downregulating the JAK2/STAT3 signaling pathway in peripheral blood, bone marrow samples, and MM cell lines [164]. Similarly, HCC cells that are resistant to chemotherapy drugs, such as docetaxel, 5-FU, and mitomycin, have higher levels of MALAT1 expression.…”

Section: The Role Of Lncrnas In Cancer Therapy Resistancementioning

confidence: 99%

Targeting miRNAs and Other Non-Coding RNAs as a Therapeutic Approach: An Update

Bayraktar

Oztatlici

et al. 2023

ncRNA

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Since the discovery of the first microRNAs (miRNAs, miRs), the understanding of miRNA biology has expanded substantially. miRNAs are involved and described as master regulators of the major hallmarks of cancer, including cell differentiation, proliferation, survival, the cell cycle, invasion, and metastasis. Experimental data indicate that cancer phenotypes can be modified by targeting miRNA expression, and because miRNAs act as tumor suppressors or oncogenes (oncomiRs), they have emerged as attractive tools and, more importantly, as a new class of targets for drug development in cancer therapeutics. With the use of miRNA mimics or molecules targeting miRNAs (i.e., small-molecule inhibitors such as anti-miRS), these therapeutics have shown promise in preclinical settings. Some miRNA-targeted therapeutics have been extended to clinical development, such as the mimic of miRNA-34 for treating cancer. Here, we discuss insights into the role of miRNAs and other non-coding RNAs in tumorigenesis and resistance and summarize some recent successful systemic delivery approaches and recent developments in miRNAs as targets for anticancer drug development. Furthermore, we provide a comprehensive overview of mimics and inhibitors that are in clinical trials and finally a list of clinical trials based on miRNAs.

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Increased lncRNA HOTAIR expression promotes the chemoresistance of multiple myeloma to dexamethasone by regulating cell viability and apoptosis by mediating the JAK2/STAT3 signaling pathway

Cited by 16 publications

References 32 publications

LncRNA PlncRNA-1 accelerates the progression of prostate cancer by regulating PTEN/Akt axis

LncRNA PlncRNA-1 accelerates the progression of prostate cancer by regulating PTEN/Akt axis

KCNQ1OT1 lncRNA affects the proliferation, apoptosis, and chemoresistance of small cell lung cancer cells via the JAK2/ STAT3 axis

Targeting miRNAs and Other Non-Coding RNAs as a Therapeutic Approach: An Update

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