miRNA-874-3p inhibits the migration, invasion and proliferation of breast cancer cells by targeting VDAC1

Yang, Housheng; Wang, Zhiwen; Hu, Shuang; Chen, Lu; Li, Wei; Yang, Zhongyi

doi:10.18632/aging.204474

Cited by 9 publications

(4 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additionally, VDAC1 has a role in cell division and apoptosis [37]. Overexpression of VDAC1 has been shown in breast cancer research to facilitate the growth, migration, and invasion of breast cancer cells [38]. Regulation of VDAC1 causes mitochondrial dysfunction and significant alterations in the signaling pathways that promote malignancy in prostate cancer [39].…”

Section: Discussionmentioning

confidence: 99%

TMCO1 regulates cell proliferation, metastasis and EMT signaling through CALR, promoting ovarian cancer progression and cisplatin resistance

Guangyu Sun,

Shan Gong,

Suwei Lan

et al. 2024

Cell Mol Biol (Noisy-le-grand)

View full text Add to dashboard Cite

This study aimed to explore the involvement of Transmembrane and coiled-coil domains 1 (TMCO1) in ovarian cancer progression and its regulatory mechanisms in cisplatin resistance. Using the GEPIA database, we analyzed TMCO1 expression in ovarian cancer and normal tissues. In a cohort of 99 ovarian cancer patients, immunohistochemistry and immunofluorescence were employed to assess TMCO1 expression in tumor and adjacent tissues, correlating findings with clinical and pathological characteristics. TMCO1 overexpression and knockout cell models were constructed, and their impact on non-cisplatin-resistant (SK-OV-3) and cisplatinresistant (SK-OV-3-CDDP) ovarian cancer cells was investigated through cloning, wound healing, Fluo 4, and Transwell experiments. Knocking down CALR and VDAC1 was performed to examine their effects on TMCO1, cell proliferation, and malignant markers. Subcutaneous tumor models in nude mice elucidated the in vivo role of TMCO1 in tumor growth. Expression levels of CALR, VDAC1, angiogenesis indicators (CD34), and epithelial-mesenchymal transition (EMT) markers were evaluated. TMCO1 expression in ovarian cancer tissue significantly differed from normal tissue, correlating with survival rates. TMCO1 overexpression was associated with lymph node metastases, late FIGO stage, and larger tumors. TMCO1 promoted proliferation, calcium ion elevation, cytoskeletal remodeling, and metastasis in SK-OV-3 and SK-OV-3-CDDP cells, upregulating VDAC1, CALR, Vimentin, N-cadherin, β-catenin, and downregulating E-cadherin. Silencing TMCO1 inhibited cell growth, proliferation, and angiogenesis in vivo, suppressing the expression of CALR, VDAC1, Vimentin, N-cadherin, and β-catenin. Overall, this study highlighted TMCO1 as a crucial regulator in ovarian cancer progression, influencing VDAC1 through CALR and impacting diverse cellular processes, offering potential as a targeted therapeutic strategy for ovarian cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

TMCO1 regulates cell proliferation, metastasis and EMT signaling through CALR, promoting ovarian cancer progression and cisplatin resistance

Guangyu Sun,

Shan Gong,

Suwei Lan

et al. 2024

Cell Mol Biol (Noisy-le-grand)

View full text Add to dashboard Cite

show abstract

“…For example, miR-144-3p can induce iron deficiency by negatively regulating the expression of ZEB1, thereby inhibiting the proliferation, migration, and invasion of osteosarcoma (OS) cells ( Jiang M. et al, 2023 ). miR-874-3p can participate in the migration, invasion, and proliferation of breast cancer cells by targeting voltage-dependent anion channel 1 (VDAC1) ( Yang et al, 2023 ). miR-223-3p regulates ECT2 to promote GC proliferation, invasion, and metastasis through the Wnt/β-catenin signaling pathway ( Li et al, 2023 ).…”

Section: Mirnamentioning

confidence: 99%

The hidden messengers: cancer associated fibroblasts—derived exosomal miRNAs as key regulators of cancer malignancy

Gou,

Li,

Liu

et al. 2024

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Cancer-associated fibroblasts (CAFs), a class of stromal cells in the tumor microenvironment (TME), play a key role in controlling cancer cell invasion and metastasis, immune evasion, angiogenesis, and resistance to chemotherapy. CAFs mediate their activities by secreting soluble chemicals, releasing exosomes, and altering the extracellular matrix (ECM). Exosomes contain various biomolecules, such as nucleic acids, lipids, and proteins. microRNA (miRNA), a 22–26 nucleotide non-coding RNA, can regulate the cellular transcription processes. Studies have shown that miRNA-loaded exosomes secreted by CAFs engage in various regulatory communication networks with other TME constituents. This study focused on the roles of CAF-derived exosomal miRNAs in generating cancer malignant characteristics, including immune modulation, tumor growth, migration and invasion, epithelial-mesenchymal transition (EMT), and treatment resistance. This study thoroughly examines miRNA’s dual regulatory roles in promoting and suppressing cancer. Thus, changes in the CAF-derived exosomal miRNAs can be used as biomarkers for the diagnosis and prognosis of patients, and their specificity can be used to develop newer therapies. This review also discusses the pressing problems that require immediate attention, aiming to inspire researchers to explore more novel avenues in this field.

show abstract

“…Numerous research has demonstrated that dysregulated ncRNAs related to metabolic networks can promote or suppress carcinogenesis, by facilitating cancer to acquire and maintain aggressive malignant phenotype and to target multiple metabolic signaling pathways [ 54 – 62 ]. Therefore, we update the latest research progress on the mechanisms of ncRNAs in metabolic reprogramming from three perspectives: glucose, lipid and amino acids, respectively.…”

Section: Ncrnas Affect Cancer Progression Through Metabolic Reprogram...mentioning

confidence: 99%

The roles and molecular mechanisms of non-coding RNA in cancer metabolic reprogramming

Li,

Peng,

Tan

et al. 2024

Cancer Cell Int

View full text Add to dashboard Cite

One of the key features of cancer is energy metabolic reprogramming which is tightly related to cancer proliferation, invasion, metastasis, and chemotherapy resistance. NcRNAs are a class of RNAs having no protein-coding potential and mainly include microRNAs, lncRNAs and circRNAs. Accumulated evidence has suggested that ncRNAs play an essential role in regulating cancer metabolic reprogramming, and the altered metabolic networks mediated by ncRNAs primarily drive carcinogenesis by regulating the expression of metabolic enzymes and transporter proteins. Importantly, accumulated research has revealed that dysregulated ncRNAs mediate metabolic reprogramming contributing to the generation of therapeutic tolerance. Elucidating the molecular mechanism of ncRNAs in cancer metabolic reprogramming can provide promising metabolism-related therapeutic targets for treatment as well as overcome therapeutic tolerance. In conclusion, this review updates the latest molecular mechanisms of ncRNAs related to cancer metabolic reprogramming.

show abstract

miRNA-874-3p inhibits the migration, invasion and proliferation of breast cancer cells by targeting VDAC1

Cited by 9 publications

References 39 publications

TMCO1 regulates cell proliferation, metastasis and EMT signaling through CALR, promoting ovarian cancer progression and cisplatin resistance

TMCO1 regulates cell proliferation, metastasis and EMT signaling through CALR, promoting ovarian cancer progression and cisplatin resistance

The hidden messengers: cancer associated fibroblasts—derived exosomal miRNAs as key regulators of cancer malignancy

The roles and molecular mechanisms of non-coding RNA in cancer metabolic reprogramming

Contact Info

Product

Resources

About