Long noncoding RNA RP11-70C1.3 confers chemoresistance of breast cancer cells through miR-6736-3p/NRP-1 axis

Zhang, Lansheng; Zheng, Xia; Shen, Anqi; Hua, Daojin; Zhu, Panrong; Li, Caihong; Han, Zhengxiang

doi:10.17305/bjbms.2021.5803

Cited by 5 publications

(4 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies have shown that patients receiving long-term chemotherapy often develop chemoresistance [ 3 ]. For example, adriamycin (ADR) is an effective chemotherapeutic drug commonly used for breast cancer treatment.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of lncRNA FOXD2-AS1 Inhibits Proliferation, Migration, and Drug Resistance of Breast Cancer Cells

Nong

et al. 2021

Computational and Mathematical Methods in Medicine

View full text Add to dashboard Cite

Objective. In order to investigate the effect of lncRNA FOXD2-AS1 on breast cancer cells proliferation, migration, and drug resistance as well as its molecular mechanism. Methods. Real-time PCR was used to detect the expression of breast cancer tissues and cells from patients admitted to our hospital and the expression of lncRNA FOXD2-AS1 in MCF-7/ADR in adriamycin- (ADR-) resistant breast cancer cells. After interfering with or overexpressing lncRNA FOXD2-AS1 in MCF-7/ADR cells, cell proliferation, apoptosis, invasion, and migration were detected using CCK-8, flow cytometry, Transwell assay, and scratch test, respectively. The protein levels of PI3K, p-PI3K, AKT, and p-AKT in the PI3K/AKT signaling pathway were detected by Western blot. Results. lncRNA FOXD2-AS1 was upregulated in breast cancer tissues and cells and increased cell drug resistance to ADR. Downregulation of lncRNA FOXD2-AS1 inhibited invasion and migration of MCF-7/ADR cells, promoted apoptosis, increased chemosensitivity of MCF-7/ADR cells, and inhibited the activity of PI3K/AKT signaling pathway in MCF-7/ADR cells. Conclusions. lncRNA FOXD2-AS1 can promote the proliferation, invasion, migration, and drug resistance of breast cancer cells, inhibit apoptosis, and accelerate the development of breast cancer by positively regulating the PI3K/AKT signaling pathway.

show abstract

Section: Introductionmentioning

confidence: 99%

Knockdown of lncRNA FOXD2-AS1 Inhibits Proliferation, Migration, and Drug Resistance of Breast Cancer Cells

Nong

et al. 2021

Computational and Mathematical Methods in Medicine

View full text Add to dashboard Cite

show abstract

“…5 The dysregulation of NRP-1 has been observed in several malignancies, such as breast cancer and bladder cancer. 6,7 Moreover, previous evidence has indicated that NRP-1 is highly expressed in GBM and plays a pivotal role in GBM progression. 8 High NRP-1 expression correlates with poor prognosis in GBM patients.…”

Section: Introductionmentioning

confidence: 99%

“…Neuropilin‐1 (NRP‐1) encodes a transmembrane glycoprotein that has been indicated to regulate axon guidance and nervous system development 5 . The dysregulation of NRP‐1 has been observed in several malignancies, such as breast cancer and bladder cancer 6,7 . Moreover, previous evidence has indicated that NRP‐1 is highly expressed in GBM and plays a pivotal role in GBM progression 8 .…”

Section: Introductionmentioning

confidence: 99%

Neuropilin‐1 enhances temozolomide resistance in glioblastoma via the STAT1/p53/p21 axis

Huang,

Zhang,

Wang

et al. 2024

Neuropathology

View full text Add to dashboard Cite

Glioblastoma (GBM) is the most prevalent primary intracranial tumor. Temozolomide (TMZ) is the first‐line chemotherapy for GBM. Nonetheless, the development of TMZ resistance has become a main cause of treatment failure in GBM patients. Evidence suggests that neuropilin‐1 (NRP‐1) silencing can attenuate GBM cell resistance to TMZ. This study aims to determine potential mechanisms by which NRP‐1 affects TMZ resistance in GBM. The parental U251 and LN229 GBM cells were exposed to increasing concentrations of TMZ to construct TMZ‐resistant GBM cells (U251/TMZ, LN229/TMZ). BALB/c nude mice were injected with U251/TMZ cells to establish the xenograft mouse model. Functional experiments were carried out to examine NRP‐1 functions. Western blotting and real‐time quantitative polymerase chain reaction were used to evaluate molecular protein and mRNA expression, respectively. Immunohistochemical staining showed NRP‐1 and STAT1 expression in mouse tumors. The results showed that NRP‐1 was highly expressed in TMZ‐resistant cells. Moreover, knocking down NRP‐1 attenuated the TMZ resistance of U251/TMZ cells, while upregulating NRP‐1 enhanced TMZ resistance of the parental cells. NRP‐1 silencing elevated GBM cell sensitivity to TMZ in tumor‐bearing mice. Depleting NRP‐1 reduced STAT1, p53, and p21 expression in U251/TMZ cells. STAT1 depletion offset NRP‐1 silencing evoked attenuation of GBM cell resistance to TMZ. Collectively, our study reveals that NRP‐1 enhances TMZ resistance in GBM possibly by regulating the STAT1/p53/p21 axis.

show abstract

“…Although lncRNAs possess no protein-coding ability, they are emerging as important players in gene silencing, transcriptional activation, chromosome modification, and intranuclear transport [6,7]. The contribution of lncRNAs in breast cancer has, therefore, received increasing attention [8][9][10]. Furthermore, many studies have provided evidence supporting lncRNA dysregulation in breast cancer and their significant roles [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA PPP1R14B-AS1 imitates microRNA-134-3p to facilitate breast cancer progression by upregulating LIM and SH3 protein 1

ZHOU¹,

ZHANG²,

Guan³

et al. 2021

Oncology Research

View full text Add to dashboard Cite

Long noncoding RNA PPP1R14B antisense RNA 1 (PPP1R14B-AS1) has emerged as a critical modulator of liver cancer and lung adenocarcinoma progression. However, the functional importance and biological relevance of PPP1R14B-AS1 in breast cancer remain unclear. Therefore, this study was designed to detect PPP1R14B-AS1 levels in breast cancer cells using qRT-PCR and elucidate the influence of PPP1R14B-AS1 on aggressive phenotypes.Furthermore, molecular events mediating the action of PPP1R14B-AS1 were characterized in detail. Functional experiments addressed the impacts of PPP1R14B-AS1 knockdown on breast cancer cells. In this study, PPP1R14B-AS1 was found to be overexpressed in breast cancer, exhibiting a close correlation with poor patient prognosis.Results also showed that breast cancer cell proliferation and motility were suppressed when PPP1R14B-AS1 was silenced. Mechanistically, PPP1R14B-AS1 acted as a competing endogenous RNA for microRNA-134-3p (miR-134-3p) in breast cancer cells. PPP1R14B-AS1 also increased LIM and SH3 protein 1 (LASP1) levels by imitating miR-134-3p in breast cancer cells. Rescue experiments further corroborated that the knockdown of miR-134-3p or an increase in LASP1 restored the aggressive malignant characteristics of breast cancer cells that were weakened by PPP1R14B-AS1 depletion. In summary, PPP1R14B-AS1 facilitated the oncogenicity of breast cancer cells by controlling the miR-134-3p/LASP1 axis. We believe that our findings may contribute to the development of precision therapy techniques in the field of breast cancer treatment.

show abstract

Long noncoding RNA RP11-70C1.3 confers chemoresistance of breast cancer cells through miR-6736-3p/NRP-1 axis

Cited by 5 publications

References 33 publications

Knockdown of lncRNA FOXD2-AS1 Inhibits Proliferation, Migration, and Drug Resistance of Breast Cancer Cells

Knockdown of lncRNA FOXD2-AS1 Inhibits Proliferation, Migration, and Drug Resistance of Breast Cancer Cells

Neuropilin‐1 enhances temozolomide resistance in glioblastoma via the STAT1/p53/p21 axis

Long noncoding RNA PPP1R14B-AS1 imitates microRNA-134-3p to facilitate breast cancer progression by upregulating LIM and SH3 protein 1

Contact Info

Product

Resources

About