Table 3 Role of PI3K/AKT pathway in esophageal squamous cell carcinoma

ESCC (n = 89), NCLM (n = 58)

TE11

–

–

miR-21, PTEN

PI3K/AKT

miR-21 through modulation of PTEN/PI3K/AKT pathway promotes invasion/migration, proliferation, cell cycle progression, and resistance to apoptosis of ESCC cells

[47]

ESCC (n = 275)

–

–

–

EGFR, ERK1/2, STAT3

AKT1

Phosphorylated AKT1 could be involved in poor prognosis in ESCC

[48]

ESCC (n = 295)

KYSE180, KYSE140, KYSE150, KYSE30, KYSE410, KYSE450, KYSE510

–

–

PAFR, c-myc, survivin,

MMP2/9,

VEGF

Dysregulation of PAFR via PI3K/AKT pathway could contribute to the progression of ESCC

[49]

–

EC109

Vitamin E succinate (VES)

0–100 µM

Bad, Bcl-2, Caspase-9, p70S6K, 4E-BP1,

PI3K/AKT, mTOR

VES via PI3K/AKT signaling pathway can activate apoptosis in ESCC

[50]

–

KYSE140, KYSE150,

KYSE30, KYSE410, KYSE450, KYSE510

Dasatinib, cisplatin

10–500 nM, 0–15 µM

Src, c-myc,

MMP-9,

VEGF

PI3K/AKT, STAT3

Dasatinib via suppressing the PI3K/AKT and STST3 pathways could improve sensitivity to cisplatin in ESCC cells

[51]

-

TE13, Eca109

–

–

miR-18a,

Cyclin-D1,

PTEN, S6K1,

pRb-S780

PI3K/AKT, mTOR

miR-18a by increasing cyclin-D1 via regulating the PTEN/PI3K/AKT/mTOR axis could promote cell proliferation of ESCC cells

[52]

nude mice, 26 pairs of ESCC and nearby non-cancerous tissues

EC109, KYSE30

–

–

Urokinase plasminogen activator (uPA), GSK-3β

PI3K/AKT, ERK

uPA realized from cancer-associated fibroblasts (CAFs) via the PI3K/AKT and ERK pathways can promote migration, invasion, and proliferation of ESCC cells

[53]

nude mice, 20 pairs of ESCC and nearby non-cancerous tissues

Eca109, TE-1, EC109, HET-1A

–

–

RUNX2, PARP, Caspase-3,

GSK-3β

PI3K/AKT,

ERK

Expression of RUNX2 by activating the PI3K/AKT and ERK pathways could play an oncogenic role in ESCC cells

[54]

–

KYSE-30

Aprepitant

0–100 µM

NF-kB

PI3K/AKT

SP/NK1R system via the PI3K/Akt/NF-kB pathway could be involved in the pathogenesis of ESCC

[55]

–

EC109, KYSE510, EC9706, NE2, COLO680N, SHEE, EC171, EC18,

EC8712

–

–

miR-200b,

E-cadherin, Vimentin,

ZEB1/2

Kindlin-2/integrin β1/AKT

miR-200b via inhibiting the Kindlin-2-integrin β1/AKT pathway could decrease invasion of ESCC cells

[56]

145 pairs of ESCC and adjacent normal tissues

–

–

–

PTEN, P70S6K1, 4E-BP1

PI3K/AKT, mTOR

PTEN low expression and induction of PI3K/AKT/mTOR signaling can increase ESCC progression

[57]

ESCC (n = 68),

TE-8, TE-9, TE-15, Het-1A

–

–

CCL3,CCR5/1, MMP2, MMP9, VEGFA

PI3K/AKT, MEK/ERK

CCL3–CCR5 axis via the MEK/ERK and PI3K/AKT pathways could promote invasion, migration, and angiogenesis of ESCC cells

[58]

BALB/c nude mice

Eca109, TE-1

–

–

HPV16 E6-E7, p75NTR

PI3K/AKT

HPV16 E6-E7 via up-regulating the p75NTR and activating the PI3K/AKT pathway could act as a cancer stem-like cells (CSCs) phenotypes promoter in ESCC cells

[59]