Direct Downregulation of B-Cell Translocation Gene 3 by microRNA-93 Is Required for Desensitizing Esophageal Cancer to Radiotherapy

Cui, Hujun; Zhang, Shengqiang; Zhou, Hongbo; Guo, Ling

doi:10.1007/s10620-017-4579-x

Cited by 17 publications

(6 citation statements)

References 29 publications

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“…Also, we further demonstrated that HOTAIR loss enhanced IR-mediated anti-tumor effects in CRC xenograft tumors. MiR-93, a member of miR-106b~25 cluster 28 , has been found to be closely linked with tumor initiation, progression, and radioresistance in some malignancies [29][30][31] . Also, previous studies showed that miR-93 could function as a negative regulator of cell autophagy 32 .…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA HOTAIR knockdown enhances radiosensitivity through regulating microRNA-93/ATG12 axis in colorectal cancer

Liu

Chen

et al. 2020

Cell Death Dis

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Colorectal cancer (CRC) is a global healthcare problem. Radioresistance is a huge setback for CRC radiotherapy. In this text, the roles and molecular mechanisms of long non-coding RNA HOTAIR in CRC tumorigenesis and radioresistance were further investigated. ATG12 mRNA, HOTAIR, and microRNA-93 (miR-93) levels were measured by quantitative reverse transcription polymerase chain reaction (RT-qPCR) assay. Protein levels of LC3 I, LC3 II, p62, ATG12, cleaved caspase 3, Bax, and Bcl-2 were detected by western blotting assay in cells and were examined by immunohistochemistry (IHC) assay in tissues. Cell survival fractions, viability, and apoptotic rates were determined by clonogenic survival assay, CCK-8 assay, and flow cytometry analysis, respectively. The relationships of HOTAIR, miR-93, and ATG12 were tested by bioinformatics analysis and luciferase reporter assay. Mouse xenograft tumor models were established to investigate the influence of HOTAIR knockdown on CRC radioresistance in vivo. We found that HOTAIR expression was markedly upregulated in plasma from CRC patients after radiotherapy and CRC cells after irradiation. HOTAIR knockdown, miR-93 overexpression, or ATG12 silencing weakened cell viability, induced cell apoptosis, inhibited cell autophagy, and enhanced cell radiosensitivity in CRC. HOTAIR exerted its functions by downregulating miR-93. Moreover, HOTAIR functioned as a molecular sponge of miR-93 to regulate ATG12 expression. ATG12 protein expression was markedly upregulated and associated with miR-93 and HOTAIR expression in CRC tissues. Furthermore, HOTAIR knockdown enhanced radiosensitivity of CRC xenograft tumors by regulating miR-93/ATG12 axis. In conclusion, HOTAIR knockdown potentiated radiosensitivity through regulating miR-93/ATG12 axis in CRC, further elucidating the roles and molecular basis of HOTAIR in CRC radioresistance.

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Section: Discussionmentioning

confidence: 99%

Long non-coding RNA HOTAIR knockdown enhances radiosensitivity through regulating microRNA-93/ATG12 axis in colorectal cancer

Liu

Chen

et al. 2020

Cell Death Dis

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“…Various miRNAs have been reported to be aberrantly expressed in a number of different types of human cancer, including miR-144 (3,29,31). miR-144 has been widely researched and reported to be an important regulator of tumor development.…”

Section: Discussionmentioning

confidence: 99%

microRNA‑144 inhibits cell proliferation and invasion by directly targeting TIGAR in esophageal carcinoma

Wang

Tan

et al. 2020

Oncol Lett

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microRNAs (miRNAs) have been identified to play vital roles in the development and progression of numerous different types of human malignancy, including esophageal squamous cell carcinoma (ESCC). In the present study, the biological function of microRNA-144 (miR-144) was investigated, as well as its underlying molecular mechanism in ESCC. The results revealed that miR-144 expression was significantly decreased, whereas the expression of TP53-inducible glycolysis and apoptosis regulator (TIGAR) was significantly increased in human ESCC tissues when compared with adjacent non-tumor tissues. An increase in TIGAR was significantly associated with tumor size and Tumor-Node-Metastasis staging in patients. Functional analysis revealed that the overexpression of miR-144 using lentivirus particles significantly inhibited cell proliferation and tumor colony formation, and induced cell apoptosis in EC9706 and EC109 cells. The autophagy activity was also enhanced by miR-144 activity. In addition, overexpression of miR-144 significantly inhibited tumor growth in vivo. In the present study, TIGAR was confirmed to be the downstream target of miR-144 in ESCC. siRNA-mediated downregulation of TIGAR inversely regulated the inhibition effect of miR-144 on ESCC cells. To conclude, the present study demonstrated that miR-144 inhibits proliferation and invasion in esophageal cancer by directly targeting TIGAR.

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“…Fortunately, we have witnessed a remarkable decrease in the incidence rate of cervical cancer due to the powerful tools in diagnosis and further therapy of this disorder [123,124]. B cell translocation gene 3 (BTG3) inhibition is a promising strategy by tumor cells to decrease the efficacy of radiotherapy [125]. Moreover, BTG3 is considered as a tumor suppressor and its inhibition enhances the malignancy of cervical cancer cells [126].…”

Section: Cervical Cancermentioning

confidence: 99%

“…MiR-93 enhances the malignancy and proliferation of glioblastoma cells by inhibition of autophagy via down-regulation of Beclin-1, ATG5, and ATG4B [106] EC cells Oncogenesis Reducing the capability of radiotherapy by inhibition of BTG3 [125] HeLa and C-33A cells cervical cancer tissues Oncogenesis LncRNA ZNF667 suppresses the invasion and malignancy of cancer cells by inhibition of miR-93-3p [311] Cisplatin-resistant A2780/DDP cell line Oncogenesis Inhibition of miR-93 by l-tetrahydropalmatine is beneficial in sensitizing of cancer cells to cisplatin-mediated apoptosis [312] Bladder cancer tissues and cells Oncogenesis Upregulation of miR-93 is related to the tumor stage and node stage via stimulation of PEDF [313] Cervical cancer and matched non-cancerous tissue samples…”

Section: Glioblastoma Cells Oncogenesismentioning

confidence: 99%

Flaming the fight against cancer cells: the role of microRNA-93

et al. 2020

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There have been attempts to develop novel anti-tumor drugs in cancer therapy. Although satisfying results have been observed at a consequence of application of chemotherapeutic agents, the cancer cells are capable of making resistance into these agents. This has forced scientists into genetic manipulation as genetic alterations are responsible for generation of a high number of cancer cells. MicroRNAs (miRs) are endogenous, short non-coding RNAs that affect target genes at the post-transcriptional level. Increasing evidence reveals the potential role of miRs in regulation of biological processes including angiogenesis, metabolism, cell proliferation, cell division, and cell differentiation. Abnormal expression of miRs is associated with development of a number of pathologic events, particularly cancer. MiR-93 plays a significant role in both physiological and pathological mechanisms. At the present review, we show how this miR dually affects the proliferation and invasion of cancer cells. Besides, we elucidate the oncogenesis or oncosuppressor function of miR-93.

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Direct Downregulation of B-Cell Translocation Gene 3 by microRNA-93 Is Required for Desensitizing Esophageal Cancer to Radiotherapy

Abstract: Direct downregulation of BTG3 by miR-93 is able to render ESC resistant to radiotherapy, and both BTG3 and miR-93 may potentially serve as clinical markers for ESC and contribute to the treatment of ESC.

Cited by 17 publications

References 29 publications

Long non-coding RNA HOTAIR knockdown enhances radiosensitivity through regulating microRNA-93/ATG12 axis in colorectal cancer

Long non-coding RNA HOTAIR knockdown enhances radiosensitivity through regulating microRNA-93/ATG12 axis in colorectal cancer

microRNA‑144 inhibits cell proliferation and invasion by directly targeting TIGAR in esophageal carcinoma

Flaming the fight against cancer cells: the role of microRNA-93

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