Table 3 Mechanistic associations of Mcl-1 in oral cancer

STAT3

Mcl-1 mRNA was upregulated by STAT3 activation. Mcl-1 protein was stabilized by Akt-mediated GSK3β inactivation

It regulates chemoresistance in OSCC.

[38]

MYB

Mcl-1 expression was dependent on MYB expression

[41]

FBW7

FBW7 mutation stabilizes Mcl-1.

[42]

LncRNA FGD5-AS1

LncRNA FGD5-AS1 acted as an oncogene by regulating Mcl-1 via sponging miR-153-3p

[43]

Alternative splicing

Mcl-1 L transcripts overexpressed in oral cancer cell lines, and it was associated with poor prognostic indicators like advanced tumor size, lymph node metastasis, decreased survival, chemoresistance, and radioresistance

[30, 45]

HOXA10 antisense RNA (HOXA10-AS)

HOXA10-AS increased the stem cell property of OSCC stem cells via miR-29a/Mcl-1/PI3K/Akt signaling pathway

[44]

Noxa

Noxa binds to and sequesters Mcl-1, which releases Bak from Bak/Mcl-1 complex to be activated. Noxa overexpression enhanced the apoptotic effects of ABT-263

[39]

USP9X

Mcl-1 is primarily degraded by the ubiquitin–proteasome pathway in OSCC. USP9X interacts with Mcl-1 and stabilizes it to prevent its degradation

[28]

Mcl-1

p-FAK was decreased by treatment with Mcl-1 siRNA, resulting in decreases in phosphorylation of MEK1/2 and MAPK

[32]

Mcl-1

Inhibition of Mcl-1 leads to cellular apoptosis via caspase cascade via Caspase-3, 9

[33]