Molecule Information

General Information of the Molecule (ID: Mol04452)

• Name: Naaladl2-as2 ,Homo sapiens
• Synonyms: Naaladl2-as2
• Molecule Type: LncRNA

Kingdom: Metazoa
Phylum: Chordata
Class: Mammalia
Order: Primates
Family: Hominidae
Genus: Homo
Species: Homo sapiens

Type(s) of Resistant Mechanism of This Molecule

  ADTT: Aberration of the Drug's Therapeutic Target

Drug Resistance Data Categorized by Drug

Investigative Drug(s) 1 drug(s) in total

Rituximab/Doxorubicin

Drug Sensitivity Data Categorized by Their Corresponding Mechanisms

Aberration of the Drug's Therapeutic Target (ADTT)

Disease Class: Diffuse large B-cell lymphoma [ICD-11: 2A81.0] [1]

• Sensitive Disease: Diffuse large B-cell lymphoma [ICD-11: 2A81.0]
• Sensitive Drug: Rituximab/Doxorubicin
• Molecule Alteration: Expression; Down-regulation
• Experimental Note: Revealed Based on the Cell Line Data
• In Vitro Model: HEK 293T cells; Kidney; Homo sapiens (Human); CVCL_0063
• In Vitro Model: U-2932 cells; Blood; Homo sapiens (Human); CVCL_1896
• In Vitro Model: OCI-LY19 cells; Bone marrow; Homo sapiens (Human); CVCL_1878
• In Vivo Model: Athymic BALB/c nude mice model; Mus musculus
• Experiment for Molecule Alteration: Fluorescence in situ hybridization assay; Small interfering RNA assay; Luciferase reporter assay; Fluorescent qPCR; Western blot assay
• Experiment for Drug Resistance: MTT assay; Drug sensitivity testing
• Mechanism Description: We observed elevated levels of NAALADL2-AS2 in DLBCL tissues. We discovered that NAALADL2-AS2 functions as ceRNA to inhibit expression of miR-34a, miR-125a, whereas overexpression of NAALADL2-AS2 indirectly upregulates expression of BCL-2. Interfering with NAALADL2-AS2 promoted apoptosis in DLBCL cells, resulting in approximately a 40% increase in sensitivity to doxorubicin and rituximab. In vivo experiments further confirmed that targeting NAALADL2-AS2 effectively suppressed tumor growth, leading to upregulation of miR-34a and miR-125a, downregulation of BCL-2, and enhanced apoptosis in DLBCL cells, which significantly improved their sensitivity to doxorubicin and rituximab by approximately 50%.

References

• Ref 1: NAALADL2-AS2 functions as a competing endogenous RNA to regulate apoptosis and drug resistance in DLBCL. Cancer Biol Ther. 2024 Dec 31;25(1):2432690.