Table 3.

Implication of EOBC deregulated microRNAs to breast cancer.

MicroRNA	Status in EOBC	Implication to Breast Cancer	Reference
miR-9	Upregulated in estrogen receptor-positive tumors in patients with age ≤ 35 years.	Previous literature suggests direct involvement of miRNA-9 in breast cancer metastasis, due to the different levels of expression through different stages of breast cancer. MTHFD2 is one of the genes targeted by miR-9, which plays a role in cell viability and anti-apoptotic activity.	[93,94]
miR-210	Upregulated in estrogen receptor-positive tumors in patients with age ≤ 35 years.	A known hypoxia-regulated microRNA, which is upregulated in normal and transformed hypoxic cells, miR-210 has been found to be vital during tumor initiation and growth by reducing mitochondrial respiration in the hypoxic microenvironment.	[95,96]
miR-106a	Upregulated in estrogen receptor-positive tumors in patients with age ≤ 35 years.	The upregulation of miR-106a has been proven to induce breast cancer cell proliferation, colony formation, migration, and invasion in vitro. Moreover, miR-106a upregulation significantly reduces breast cancer cell apoptosis and sensitivity to cisplatin.	[97]
miR-106b	Upregulated in estrogen receptor-positive tumors in patients with age ≤ 35 years.	Breast cancer patients frequently had upregulated level of miR-106b in tissue. miR-106b expression significantly correlated with breast cancer tumor size and marker of proliferation Ki67 expression. High miR-106b expression was associated with shorter disease-free survival and overall survival in breast cancer patients.	[98]
miR-18b	Upregulated in estrogen receptor-positive tumors in patients with age ≤ 35 years.	miR-18b is involved in the modulation of breast cancer cell migration and metastasis in vitro.	[99]
miR-33b	Upregulated in estrogen receptor-positive tumors in patients with age ≤ 35 years.	miR-33b is frequently downregulated in breast cancer tissue in comparison to normal adjacent tissue. A previous study recognized miR-33b as a negative regulator for metastasis and breast cancer cell stemness.	[100]
miR-518a-3p	Upregulated in estrogen receptor-positive tumors in patients with age ≤ 35 years.	Expression of miR-518a-3p was associated with cell proliferation in several malignancies. miR-518a-3p expression was positively correlated with overall survival in triple-negative breast cancer patients.	[101]
miR-372	Downregulated in estrogen receptor-positive tumors in patients with age ≤ 35 years.	Frequently overexpressed in breast tumor tissue. Downregulation of miR-372 significantly inhibited cell proliferation and induced apoptosis of breast cancer cells.	[102]
hsa-miR-1228*	Deregulated in young age breast cancer patients (≤ 35 years).	miR-1228 plays a vital role in the regulation of cell proliferation and metastasis in cancer cells.	[103,104]
hsa-miR-3196	Deregulated in young age breast cancer patients (≤ 35 years).	Few studies elucidate the role of hsa-miR-3196 in cancer progression. However, miR-3196 was downregulated in basal cell carcinoma compared with non-lesional skin.	[105]
hsa-miR-1275	Deregulated in young age breast cancer patients (≤35 years).	Upregulated miR-1275 has been reported to induce p53 signaling pathway via regulating serpin family E member 1(SERPINE1) (which is member in P53 signalling pathway and is also a known protein involved in cell adhesion) that suppresses tumour cells proliferation, invasion, and migration while at the same time, promoting cell apoptosis. (In vitro and in vivo study in glioma). Another role for hsa-miR-1275 is to inhibit adipogenesis in obesity.	[106,107,108]
hsa-miR-1207-5p	Deregulated in young age breast cancer patients (≤35 years).	Low expression of 1207-5p targeted mRNA was reported to regulate tumor protein p53, transforming growth factor β (TGF-b) and insulin signaling pathways in metabolic syndrome patients. P53, TGF-b, and insulin signaling pathways are implicated in the initiation, progression, and metastasis of breast cancer.	[109]
hsa-miR-92b	Deregulated in young age breast cancer patients (≤35 years).	Has-miR-92b expression inhibits breast cancer cell viability, invasion, migration, and control autophagy through histone methyltransferase enhancer of zeste homolog 2 (EZH2) in vitro.	[110]
hsa-miR-139-5p	Deregulated in young age breast cancer patients (≤35 years).	hsa-miR-139-5p expression induces apoptosis and arrests cell cycle in S phase. Furthermore, it inhibits viability, migration, and invasion in breast cancer cells via targeting Notch signaling pathway.	[111]
miR-1285-5p	Correlated with overall survival in young age breast cancer patients (≤35 years).	miR-1285-5p suppresses breast cancer cell proliferation activity via upregulation of targeted gene transmembrane protein 194A (TMEM194A).	[112]
miR-183-5p	Correlated with overall survival in young age breast cancer patients (≤35 years).	miR-183-5p have oncomiR effects on breast cancer cells. Overexpression of miR-183-5p can significantly induce breast cancer cell proliferation and inhibit apoptosis in vitro.	[113]
miR-194-5p	Correlated with overall survival in young age breast cancer patients (≤35 years).	miR-194-5p were found to be upregulated in breast cancer tissue. Knockdown of miR-194-5p in breast cancer cell resulted in inhibition of cell proliferation, migration, and invasion via expression of SOX17 and regulation of the canonical Wnt (Wnt/β-catenin) signaling pathway.	[114]