Molecule Information
General Information of the Molecule (ID: Mol01454)
Name |
hsa-mir-128
,Homo sapiens
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Synonyms |
microRNA 128-2
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Molecule Type |
Precursor miRNA
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Gene Name |
MIR128-2
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Gene ID | |||||
Location |
chr3:35744476-35744559[+]
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Sequence |
UGAGCUGUUGGAUUCGGGGCCGUAGCACUGUCUGAGAGGUUUACAUUUCUCACAGUGAAC
CGGUCUCUUUUUCAGCUGCUUC Click to Show/Hide
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Ensembl ID | |||||
HGNC ID | |||||
Precursor Accession | |||||
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Type(s) of Resistant Mechanism of This Molecule
EADR: Epigenetic Alteration of DNA, RNA or Protein
Drug Resistance Data Categorized by Drug
Approved Drug(s)
3 drug(s) in total
Cisplatin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Epigenetic Alteration of DNA, RNA or Protein (EADR) | ||||
Disease Class: Lung cancer | [1] | |||
Resistant Disease | Lung cancer [ICD-11: 2C25.5] | |||
Resistant Drug | Cisplatin | |||
Molecule Alteration | Expression | Up-regulation |
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Experimental Note | Revealed Based on the Cell Line Data | |||
Cell Pathway Regulation | PI3K/AKT signaling pathway | Activation | hsa04151 | |
In Vitro Model | H1299 cells | Lung | Homo sapiens (Human) | CVCL_0060 |
A459 cells | Lung | Homo sapiens (Human) | CVCL_0023 | |
H1299 clone 23 cells | Lung | Homo sapiens (Human) | N.A. | |
H1299 clone 41 cells | Lung | Homo sapiens (Human) | N.A. | |
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Flow cytometry assay | |||
Mechanism Description | The expression of the transcriptional repressor E2F5, a target of miR-128-2, strongly decreases after miR-128-2 exogenous expression. This leads to the abrogation of E2F5 repressive activity on p21waf1 promoter and, consequently, to the transcriptional induction of p21waf1. The newly synthesized p21waf1 protein is mainly localized into the cytoplasmic compartment, where it exerts an anti-apoptotic function in response to anticancer drug treatments. |
Doxorubicin
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Epigenetic Alteration of DNA, RNA or Protein (EADR) | ||||
Disease Class: Lung cancer | [1] | |||
Resistant Disease | Lung cancer [ICD-11: 2C25.5] | |||
Resistant Drug | Doxorubicin | |||
Molecule Alteration | Expression | Up-regulation |
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Experimental Note | Revealed Based on the Cell Line Data | |||
Cell Pathway Regulation | PI3K/AKT signaling pathway | Activation | hsa04151 | |
In Vitro Model | H1299 cells | Lung | Homo sapiens (Human) | CVCL_0060 |
A459 cells | Lung | Homo sapiens (Human) | CVCL_0023 | |
H1299 clone 23 cells | Lung | Homo sapiens (Human) | N.A. | |
H1299 clone 41 cells | Lung | Homo sapiens (Human) | N.A. | |
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Flow cytometry assay | |||
Mechanism Description | The expression of the transcriptional repressor E2F5, a target of miR-128-2, strongly decreases after miR-128-2 exogenous expression. This leads to the abrogation of E2F5 repressive activity on p21waf1 promoter and, consequently, to the transcriptional induction of p21waf1. The newly synthesized p21waf1 protein is mainly localized into the cytoplasmic compartment, where it exerts an anti-apoptotic function in response to anticancer drug treatments. |
Fluorouracil
Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
Epigenetic Alteration of DNA, RNA or Protein (EADR) | ||||
Disease Class: Lung cancer | [1] | |||
Resistant Disease | Lung cancer [ICD-11: 2C25.5] | |||
Resistant Drug | Fluorouracil | |||
Molecule Alteration | Expression | Up-regulation |
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Experimental Note | Revealed Based on the Cell Line Data | |||
Cell Pathway Regulation | PI3K/AKT signaling pathway | Activation | hsa04151 | |
In Vitro Model | H1299 cells | Lung | Homo sapiens (Human) | CVCL_0060 |
A459 cells | Lung | Homo sapiens (Human) | CVCL_0023 | |
H1299 clone 23 cells | Lung | Homo sapiens (Human) | N.A. | |
H1299 clone 41 cells | Lung | Homo sapiens (Human) | N.A. | |
Experiment for Molecule Alteration |
qRT-PCR | |||
Experiment for Drug Resistance |
Flow cytometry assay | |||
Mechanism Description | The expression of the transcriptional repressor E2F5, a target of miR-128-2, strongly decreases after miR-128-2 exogenous expression. This leads to the abrogation of E2F5 repressive activity on p21waf1 promoter and, consequently, to the transcriptional induction of p21waf1. The newly synthesized p21waf1 protein is mainly localized into the cytoplasmic compartment, where it exerts an anti-apoptotic function in response to anticancer drug treatments. |
References
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