Table 1 Expression of miR-16-5p or its partners in cell lines (∆: knock-down or deletion, TIIA: Tanshinone IIA, CuET: diethyldithiocarbamate-copper complex, EPCs: endothelial progenitor cells, RANKL: receptor activator of nuclear factor-κB ligand, IDH: Isocitrate dehydrogenase)

Neuroblastoma

MYCN

SK-N‐BE(2), NB‐19, and SH‐EP Tet21N

↑↑ miR-16-5p: ↓ proliferation, migration, and invasion

[7]

Circ-CUX1, DMRT2

HUVEC, GI-LI-N, SK-N-SH and IMR-32

∆ Circ-CUX1 (which suppresses miR-16-5p): ↓ proliferation, migration, invasion , and glycolysis

[8]

Osteosarcoma

Smad3

hFOB1.19, MG63, SaOS2, HOS, and U2OS

↑↑ miR-16-5p: ↓ proliferation, migration, invasion, and ↑ therapeutic effect of cisplatin

[9]

TSPAN15, PI3K/AKT signaling pathway

hFOB 1.19, MG63, Saos2 and HOS

↑↑ miR-16-5p: ↓ viability, migration, invasion

[10]

LINC00662, ITPR1

U2OS, SAOS-2, 143B, and MG63, HFOB 1.19

∆ LINC00662 (which sponges miR-16-5p): ↓ proliferation, migration, invasion , and stemness property maintenance

[23]

hsa_circ_0005721, TEP1

hFOB, 143B, U-2OS, HOS and Saos-2

∆ hsa_circ_0005721 (which sponges miR-16-5p): ↓ viability, migration, invasion

[24]

Hepatocellular carcinoma

AGAP2-AS1, ANXA11, AKT signaling

LO2, Hep3B, HCCLM3, Huh7, MHCC-97 H and SMMC-7721

↑↑ AGAP2-AS1: ↑ proliferation, migration, invasion , and ↓ apoptosis

[11]

IGF1R

SMMC-7721, HL-7702

↑↑ miR-16-5p: ↓ proliferation, migration, invasion, and EMT process

[12]

TTN-AS1, cyclin E1, PTEN/Akt signaling pathway

Bel7404 and HepG2

∆ TTN-AS1 (which sponges miR-16-5p): ↓ sorafenib resistance, ↑ apoptosis

∆ miR-16-5p: ↑ sorafenib resistance, ↓ apoptosis

[13]

SNHG22, EZH2, DNMT1

HLE-3, Huh7, HCCLM6, MHCC97H and SNU-398

∆ SNHG22

(which suppresses the transcription of miR-16-5p): ↓ proliferation, invasion, and angiogenesis

∆ miR-16-5p: ↑ proliferation, migration, invasion, and angiogenesis

[14]

Cervical cancer

CARM1

HeLa, C-33 A, CaSki, HeLa229, SiHa, END1/

E6E7

↑↑ miR-16-5p: ↓ colony formation, and radioresistance, ↑ apoptosis

[15]

PDK4

HeLa, SiHa, HeLa/Dox, and SiHa/Dox

↑↑ miR-16-5p: ↓ proliferation, glucose consumption, lactate production, and ATP levels, and resistance to Dox treatment

[16]

DLX6-AS1, ARPP19

End1/E6E7, SiHa, HeLa, C-33 A, and CaSki

∆ DLX6-AS1 (which sponges miR-16-5p): ↓ proliferation, migration, and EMT process, ↑ apoptosis

[25]

Breast cancer

AKT3, NF-κB pathway

BT-549 and MCF-7

↑↑ miR-16-5p: ↓ proliferation, migration, ↑ apoptosis, cell cycle arrest

[17]

ANLN

MCF-7, T47D, MDA-MB-231, EMF-192 A, SKBR-3 and MCF-10 A, HEK293T

↑↑ miR-16-5p: ↓ proliferation, migration, invasion, and ↑ apoptosis, G2/M phase arrest

[18]

VEGFA , Hypoxia-inducible factor-α (HIF-α)

MCF-7 and MDA-MB-231, MDA-MB-435, MDA-MB-468 and T47D, MCF10A

↑↑ miR-16-5p: ↓ proliferation, invasion, colony formation, ↑ apoptosis

[19]

ATXN8OS, VASP

MCF-10 A MCF-7, and BT-549

∆ ATXN8OS (which sponges miR-16-5p): ↑ tamoxifen sensitivity

[20]

Gliomas

WEE1,

CHEK1 and MCL1

A172, T98G, U251MG, U138MG and U87MG, TP365MG

↑↑ miR-16-5p: ↓ proliferation, viability, ↑ apoptosis, cell cycle arrest, response to irradiation and

chemotherapy

histone deacetylase inhibitor TS treatment: ↑ miR-16-5p

∆ HDAC3: ↑ miR-16-5p

[21]

TLN1

T98G and A172

TIIA treatment: ↑ miR-16-5p

↑↑ miR-16-5p: ↓ proliferation, migration, invasion

[22]

Neuroendocrine tumors

SSTR2

INS-1 rat insulinoma cell line and GH3 rat pituitary GH- and PRL-producing cell line

octreotide treatment: ↑ miR-16-5p

↑↑ miR-16-5p: ↓

Proliferation, ↑ SSTR2 expression

[26]

Chordoma

Smad3

U-CH1 and U-CH2

↑↑ miR-16-5p: ↓ proliferation, migration, invasion

[27]

LINC00662, RNF144B

U-CH1 and U-CH2

∆ LINC00662 (which sponges miR-16-5p): ↓ proliferation, migration, invasion, colony formation, and EMT process

[28]

Gastric cancer

PD-L1

PBMCs and CD3+ T cells

AGS and NCI-N87

M1 Macrophage-Secreted Exosomes Carrying miR-16-5p: ↑ polarization of macrophages to its M1 phenotype, and T cell activation, ↓ PD-L1 expression

[29]

Smad3

BSG823 and SGC-7901

Melatonin treatment: ↑ miR-16-5p: ↓ proliferation, ↑ apoptosis

[30]

LINC00649, YAP1, Hippo signaling pathway

MGC-803 and SGC-7901

∆ LINC00649 (which sponges miR-16-5p): ↓ proliferation, migration, viability, ↑ apoptosis

[31]

LINC00473, CCND2

BGC823, AGS, MKN-45, NCI-N87, GES-1

∆ LINC00473 (which sponges miR-16-5p): ↓ proliferation, migration, invasion, ↑ apoptosis, cell arrest

[32]

Lung cancer

WEE1

GLC-82 and HTB-182

Quercetin: ↑ miR-16-5p

↑↑ miR-16-5p: ↓ proliferation, colony formation, viability, ↑ apoptosis, and radiosensitivity

[33]

Linc00210, PTK2

BEAS-2B, A549, Calu-3, H1299, SPCA-1, and PC-9

∆ Linc00210 (which sponges miR-16-5p): ↓ proliferation, invasion, ↑ apoptosis

[34]

XIST, WEE1

H157, HCC827, A549 and H838

∆ XIST (which sponges miR-16-5p): ↓ colony formation, viability, ↑ apoptosis, and radiosensitivity

[35]

Colorectal cancer

PVT1, VEGFA, VEGFR1, AKT

signaling

FHC, HCT116 and SW480, and HEK293T

∆ PVT1 (which sponges miR-16-5p): ↓ proliferation, migration, and invasion

↑↑ miR-16-5p: ↓ proliferation, migration, and invasion

[36]

ALDH1A3, PKM2

HCT116, LoVo, DLD1 and RKO

CuET treatment: ↑ miR-16-5p and miR-15b-5p: ↓ glycolysis, viability and ↑ G2/M-phase arrest and apoptosis

∆ ALDH1A3 (a target of mir-16-5p): ↓ viability and clonogenicity

[37]

ITGA2

Caco-2, SW480,

SW620, LoVo, and HT29

↑↑ miR-16-5p: ↓ proliferation, migration, and invasion, ↑ apoptosis

∆ miR-16-5p: ↑ proliferation, migration, and invasion, ↓ apoptosis

[38]

Erythroleukemia

MEL cells

↑↑ miR-16-5p: ↑ erythroid differentiation of MEL cells by regulating ribosome biogenesis

[39]

Prostate cancer

AKT3

↑↑ miR-16-5p: ↓ cell survival, ↑ cell cycle distribution and apoptosis

[40]

Cyclin D1/E1-pRb-E2F1 pathway

LNCaP

Ionizing radiation: ↑ miR-16-5p: ↓ proliferation, viability, and ↑ G0/G1 phase arrest

[41]

Chondrosarcomas

VEGF-A, PI3K/Akt signaling

JJ012, SW1353

Resistin treatment: ↓ miR-16-5p: ↑ VEGF-A-dependent EPCs angiogenesis

[42]

Giant cell tumor of bone

BMM cells

↑↑ miR-16-5p: ↓ RANKL-induced osteoclastogenesis

[43]

Papillary thyroid carcinoma

SNHG12

PTC cell lines

∆ SNHG12 (which sponges miR-16-5p): ↓ proliferation, migration and invasion and ↑ apoptosis

[44]

Renal cell carcinoma

PVT1

HK-2, A498, 786-O, ACHN and Caki-1

∆ PVT1 (which sponges miR-16-5p): ↓ proliferation, migration invasion, EMT process, and ↑ apoptosis

∆ miR-16-5p: ↑ proliferation, migration invasion, EMT process, and ↓ apoptosis

[45]

Bladder cancer

BIMP1/NFκB signaling pathway

T24 and 5637

↑↑ miR-16-5p: ↓ viability, ↑ autophagy and apoptosis

[46]

LINC00649, JARID2

HCV-29, UMUC2, SW780, and T24

∆ LINC00649 (which sponges miR-16-5p): ↓ proliferation, migration, and invasion

[47]

Cholangiocarcinoma

R-2HG, ERα, YAP1

QBC939, HuCCT1, and HEK293T

IDH mutations: ↑ R-2HG production

↑ R-2HG: ↑ degradation of FTO so ↓ protein translation of the ERα: ↑ miR-16-5p: ↓ YAP1: ↓ proliferation and cell growth

[48]