Table 1 Summary of miRNAs involved in regulating autophagy in human breast cancer (n = 41)

Promote both tumorigenesis and autophagy

miR-23a

In vitro secondary cell lines (MDA-MB-231, MDA-MB-453, T47D, SKBR3, BT549, MCF-10A and MCF-7); in vivo female Balb/c nude mice study (n = unclear for each group)

Overexpression of miR-23a downregulated (p < 0.05) XIAP expression and this promoted autophagy and breast cancer tumorigenesis in vitro and in vivo

[96]

miR-23b-3p

In vitro secondary cell lines (MCF-7, ZR-75-1 and HCC1428); in vivo female Balb/c nude or NSG/NOD mice study (n = 4 for each group)

Downregulation of SLC6A14 by miR-23b-3p caused increased influx of acidic amino acids in the endocrine therapy resistant breast cancer cells and this promoted autophagy and tumorigenesis

[35]

miR-126

Clinical sampling (breast cancer patients = 106); in vitro secondary cell lines (MCF-7 and MDA-MB-231); in vivo female Balb/c nude mice study (n = 9 for each group)

Overexpression of miR-126 downregulated IRS/Glut-4 signaling pathway and activated AMPK/autophagy pathway to promote tumorigenesis

[86]

miR-638

In vitro secondary cell lines (KYSE450 ESCC and MCF-7); clinical sampling (breast cancer samples = 24, esophageal cancer tissues = 66)

Upregulation of miR-638 would significantly downregulate (p < 0.05) DACT3 expression, which then promoted autophagy and tumorigenesis in both breast and esophageal cancers

[81]

Promote autophagy but suppress tumorigenesis

miR-125b-5p

In vitro secondary cell lines (MCF-7); in vivo female Balb/c nude mice study (n = 6 for each group)

MiR-125b-5p negatively regulated PAD2 (p < 0.05) and this sensitized the breast cancer cells to tamoxifen and docetaxel treatment by accelerating apoptosis and autophagy

[66]

Suppress autophagy but promote tumorigenesis

miR-20a

Online clinical data (breast cancer = 694, normal = 83); clinical sampling (n = 30 for cancer or normal tissues); in vitro secondary cell lines (MDA-MB-231 and MCF-7); in vivo female Balb/c nude mice study (n = 12 for each group)

miR-20a level was negatively correlated to BECN1, ATG16L1 and SQSTM1 expression level. Elevated miR-20a increased DNA mutation and tumorigenesis by decreasing autophagy activities

[74]

miR-21

In vitro secondary cell line (MCF-7)

Knockdown of miR-21 would enhance autophagy and improve breast cancer cells sensitivity to tamoxifen and fulvestrant by inhibiting PI3K/AKT/mTOR pathway

[75]

miR-25

In vitro secondary cell lines (MCF-7 and MCF-10A); in vivo female NOD/SCID mice (n = 6 for control or treated group)

Upregulation of miR-25 reduced autophagy by reducing ULK1 expression (p < 0.05). This led to chemoresistance

[68]

Suppress autophagy but promote tumorigenesis

miR-96-5p

In vitro secondary cell lines (MDA-MB-231, MCF-7, BT-549, HS578T, T47D, ZR-75-1 and MCF-10A)

Overexpression of miR-96-5p significantly suppressed (p < 0.05) autophagy and apoptosis, and increased tumorigenesis

[83]

miR-137

In vitro secondary cell lines (SKBR3, MCF-7 and MDA-MB-231)

Overexpression of miR-137 significantly (p < 0.05) apoptosis and autophagy and promoted cancer cells tumorigenesis

[99]

miR-221

In vitro secondary cell lines (MDA-MB-231, MCF-7, T47D, ZR-751, SKBR-3 and HMEC); in vivo athymic female mice (n = 5 for each group)

Elevation of miR-221 downregulated beclin-1 (p < 0.05) in vitro and in vivo. This caused reduced autophagy but increased tumorigenesis and cancer aggressiveness

[76]

miR-224-5p

Clinical sampling (metastatic breast cancer = 30, non-metastatic breast cancer = 35, normal control = 25); in vitro secondary cell lines (MDA-MB-231 and MCF-7)

Introduction of miR-224-5p suppressed autophagy by reducing Smad4 expression (p < 0.05). High miR-224-5p level was found in metastatic breast cancer patients than normal control or patients with non-metastatic lesions

[101]

miR-486-5p

In vitro secondary cell lines (MCF-7 and MDA-MB-231)

Upregulation of miR-486-5p would downregulate PTEN expression (p < 0.05) and autophagy but enhanced AKT signaling pathway

[56]

Suppress autophagy but promote tumorigenesis

miR-638

Case–control (breast cancer or normal control, each had 47 samples); bioinformatics target prediction

Downregulation of miR-638 might be associated with good disease prognosis and slow disease prognosis by increasing autophagy activity

[79]

Suppress both autophagy and tumorigenesis

Let-7a

Un-reported

In vitro secondary cell line (MDA-MB-231)

Overexpression of Let-7a significantly (p < 0.05) increased apoptosis, reduced autophagy, and cell proliferation in vitro

[102]

miR-20a

miR-20b

Clinical sampling (breast cancer tissues and normal tissues = 19); in vitro secondary cell lines (MCF-7, MCF-10A and MDA-MB-231)

Overexpression of miR-20a and miR-20b suppressed (p < 0.05) autophagy and tumorigenesis

[72]

miR-26b

Clinical sampling (breast cancer tissues and normal tissues = 3); in vitro secondary cell line (MCF-7)

Increased expression of miR-26b downregulated DRAM1 protein expression in breast cancer cell and this reduced autophagy and sensitized cancer cells to irradiation

[92]

miR-27a

In vitro secondary cell lines (MDA-MB-231 and MCF-7)

Introduction of antagonist of miR-27a increased (p < 0.05) LC3-II and p62 expression in vitro, increased autophagy and chemoresistance

[82]

Suppress both autophagy and tumorigenesis

miR-101

In vitro secondary cell line (MCF-7)

Overexpression of miR-101 downregulated STMN1, RAB5A and ATG4D. This inhibited autophagy and promoted tamoxifen (4-OHT) induced cells apoptosis

[80]

miR-107

Clinical sampling (breast cancer patients = 62); in vitro secondary cell lines (MDA-MB-231, MDA-MB-453, MCF-10A and MCF-7); in vivo female Balb/c nude mice study (n = 5 for each group)

In breast cancer tissues and cell lines, miR-107 was downregulated (p < 0.01) and this was associated with increased tumorigenicity. Overexpression of miR-107 downregulated HMGB1 in vitro and in vivo and inhibited autophagy

[36]

miR-129-5p

In vitro secondary cell line (MCF-7)

Upregulation of miR-120-5p significantly suppressed (p < 0.05) HMGB1 expression. This led to autophagy downregulation and increased chemosensitivity against taxol

[61]

miR-200c

Clinical sampling (breast cancer patients = 35); in vitro secondary cell lines (MDA-MB-231, BT549, BT474, MCF-10A and MCF-7)

Ectopic expression of miR-200c downregulated UBQLN1 and this blocked radiation-induced autophagy and sensitized cancer cells to radiotherapy

[93]

Suppress both autophagy and tumorigenesis

miR-489

In vitro secondary cell line (T47D, MCF-7, MDA-MB-231, MDA-MB-468, MDA-MB-361, Hs578T and ZR-75-1); in vivo athymic female mice (n = 5 for each group); clinical sampling (breast cancer patients = 14)

In vitro and in vivo findings suggested that upregulation of miR-489 downregulated ULK1 and LAPTM4B, which then suppressed autophagy and increased cancer cells sensitivity towards doxorubicin

[37]

miR-567

Clinical sampling (breast cancer tissues = 98); in vitro secondary cell lines (SKBR3 and BT474); in vivo male Balb/c nude mice study (n = 4 for each group)

Introduction of miR-567 downregulated ATG5 expression in vitro and in vivo, and this suppressed autophagy and sensitized cancer cells to trastuzumab

[78]

miR-1275

Clinical sampling divided into 3 cohorts (breast cancer samples = 161, normal tissues = 127); in vitro secondary cell lines (MDA-MB-231 and MCF-7); in vivo Balb/c nude female mice (n = 6 for each group)

Overexpression of miR-1245 would downregulate ATG7 and ULK1 in vitro and in vivo, which then suppressed autophagy and tumorigenesis. Downregulation of miR-1275 by circCDYL in breast cancer patients led to poor survival

[69]

Suppress both autophagy and tumorigenesis

miR-30c-1

miR-149

miR-611

miR-615-5p

miR-659

miR-636

miR-638

miR-659

miR-675

miR-1303

miR-1308

miR-1908

miR-1914

miR-1915

miR-2861

miR-3184

miR-4292

miR-4259

In vitro secondary cell line (MDA-MB-231)

Introduction of BIK interference would result in the upregulation of a number of autophagy-regulating miRNAs which were shown to regulate several key autophagy-related proteins like ULK1/2, LC3-II and MAPK3

[67]